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October 24, 2011

When Practice Won't Make Perfect

Catherine Waymel

As CU students well know, learning takes time. Sometimes it may entail incessant reading or repeating a single definition 20 times in a row, but eventually it pays off (at least until after the test). But what if you had to repeat that definition 100 times? 200? 300? Well for those who have Down syndrome this happens to be the case.

Down syndrome (or trisomy 21) is a phenomenon in which a person has 3 copies of the 21st chromosome. This results in a distinct phenotype which includes deficiencies in learning and memory. My youngest sister has Down syndrome, and I know from experience that the most prominent manifestation of slower learning is the need for substantial repetition. I remember spending countless summer hours when I was 11 teaching my sister the ABCs--and not yet comprehending the full implications of Down syndrome I was puzzled at the amount of reiteration necessary. Now studies are finally discovering the biological basis for this detained memory.

In a study published by the Journal of Neuroscience in 2004, researchers from
Standford Medical, Stanford University, and the University of California in San Francisco explored the disparity in learning between Down syndrome and non-syndrome brains. In studying the hippocampus of a genetic mouse model for Down syndrome (Ts65Dn), they discovered that Long Term Potentiation, the predominant mechanism for learning, was suppressed by increased inhibition.

In the study, transverse hippocampal slices of Ts65Dn and of the 2N control mice were studied in various methods. In the first trial, the cells of the dentate gyrus received a tetanus of stimuli. In the 2N mice this resulted in classic LTP as indicated by the significantly elevated post-tetanus synaptic potential. However in the Ts65Dn mice the post-synaptic potential fundamentally remained the same, displaying no significant change to its baseline potential (i.e. no LTP).

A second trial was run with paired pulses which produced a steady no-change PSP in the cells of the 2N mice but yielded a depressed PSP in the Ts65Dn mice, supporting the hypothesis of increased inhibition (not only in magnitude, but as a function of time as well). In the third trial the researchers applied picrotoxin, an inhibitor of GABA receptors, to the dentate gyrus. As a result, LTP was finally induced in the Ts65Dn mice.

The researchers concluded that increased inhibition (either a result of significantly stronger inhibition feedback loops or a greater number of inhibitory synapses) was restraining the depolarization of the post-synaptic membrane, effectively muting NMDA receptors. The picrotoxin facilitated post-synaptic depolarization enough to adequately activate the NMDA receptors, generating LTP.

For decades scientists have made very few inroads into effective treatments for cognitive deficiencies--primarily because the neurological basis has remained a mystery. But with the goal of enhancing memory and focusing the learning capabilities of those with Down syndrome I am confident that these studies will markedly increase our comprehension of how to best teach those with disabilities. In the mean time, the next time you ace a test--thank your LTP.

Kleschevnikov, Alexander et al. "Hippocampal Long-Term Potentiation Supressed by Increased Inhibition in the Ts65Dn Mouse, a Genetic Model of Down Syndrome." The Journal of Neuroscience. 15 September 2004: 8153-8160.

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Biased Perceptions: Seeing Only What Has Been Learned to See

With so many stimuli constantly around us, it would make sense that we would miss observing a lot of the world. One person may notice a hawk flying overhead where another wouldn�??t even think to look in the sky. Why is this? Why when two people are capable of observing a hawk, only one actually notices it? According to Dr. Jennifer Summerfield and colleagues, it is because the brain is biased based off of long-term memory learning. We see what we see because we have learned to see it.

To prove this theory, Summerfield conducted some experiments to observe what people look at. Participants in the study were given a series of pictures containing various scenes and asked to find a small key hidden within the picture. As the participants continued to practice searching for keys, the time it took to find them in the next picture decreased. This shows that as the brain practices searching for certain items, it will learn how to find it quicker in a new scenario. In other words, the brain is learning to find the keys quicker with each trial.

Participants were also hooked up to a machine that could trace the movements of the eyes as they looked at the pictures. During this experiment, they were once again asked to look at pictures, some of which contained a small key where others did not. The first time a participant was shown a picture containing a key, the eye movement was random as they searched for it. When they were shown the same picture for a second time, the eyes looked right at the key first and then strayed from that point. The same experiment was done, but this time with a picture not containing a key, also known as a neutral stimulus. The first time the picture was shown, the eye movement was random, as was the same as the photo containing the key. When the photo without the key was later shown again, the eyes did not target a specific point, instead the eye movement was still random, just like the first time the photo was viewed. Simply because the brain had no specific goal to look for something, they eye movement remained random. When the brain learned where the key was, it automatically looked there first.

To return on the question as to why one person would notice a hawk in the sky, while another may not, could be due to long-term potentiation of memory. The person who observed the hawk may have had past experiences that taught that person to look in the sky, where the second person did not. This brings up some thoughts on how we observe our lives. Are we always looking at the same things day to day simply because we have learned to look at those things? What parts of the world have we missed because we never had reason to notice? Perhaps through reading this, and becoming aware of the possible limitations of what we observe, as well as what is not, we can begin to see new things and as a result, create a new, broader perception.

Summerfield J, Anling R, Garside N, Nobre A (2011) Biasing Perception by Spatial Long-Term Memory. The Journal of Neuroscience 31:14952-14960
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Napping, the Legal Study Aide

Spending the entire night studying is not a novel concept for most college kids these days. The daunting task of studying for midterms and finals is a vicious cycle that lasts throughout the semester. Even if you have paid attention in class and completed all the homework, a midterm requires mass amounts of review, often in a short amount of time. Though staying up all night to maximize study time may seem like the answer for memorizing material, according to Harvard Medical School its not; and who really wants to mess with Harvard Medical School?

So what do you need to know about sleep? Sleep is classified by two different types: non-rapid eye movement (NREM) and rapid eye movement (REM). NREM is further separated into four different stages, each being a deeper form of sleep than the last. Throughout the night a person experiences many sleep cycles consisting of NREM and REM sleep, with each cycle lasting 60-90 minutes.

Like sleep, memory is classified into different types, either declarative or nondeclarative. Declarative memory is conscious memory of fact-based information that can take the form of episodic or semantic memory. Nondeclarative memory is said to be unconscious, consisting of procedural memory and implicit memory.

Continuing with the exciting theme of subcategories, the development of memory takes place in stages. The first stage being the initial formation of the memory after encountering an object or performing an action, and the second being the consolidation of the memory, which works to stabilize and enhance it. The enhancement stage of consolidation occurs during sleep.

Studies have shown that REM sleep induces a brain state in which access to weak associations is selectively facilitated, and flexible, creative processing of acquired information can be enhanced (Walker 123). It has been suggested that during stage 2 of NREM sleep, sleep spindles provide depolarizing inputs into targets in the neocortex that are similar to spike trains used experimentally to induce long-term synaptic potentiation. Electrophysiological studies backed this proposed mechanism by showing that impulse trains similar to those produced by sleep spindles produce lasting changes in their responsiveness (Walker 126). Multiple other studies have shown correlations between REM and stage 2 NREM sleep with increased performance on a myriad of motor, pitch memory, and other procedural tasks. More interesting is the finding that 60-90 minute naps that contain both REM and SWS (slow-wave-sleep that occurs during stages 3 and 4 of NREM sleep) can provide the same enhancement as a normal night of sleep (Walker 124).

There is still many questions surrounding sleep-dependent memory, but there is no doubt that there is a connection. Though it is hard to think that you're going to be able to get a full 8 hours during finals week, taking a 90 minute nap is hardly unreasonable. Getting the right amount of the right type of sleep can do great things for your memory and ability to perform procedural tasks. Napping may have ended in kindergarten, but it needs to be resurrected in college.

Walker, Matthew. "Sleep-Dependent Learning and Memory Consolidation." Neuron. 30 Sep 2004: 121-133. Print.
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Vitamin D deficiency and musculoskeletal pain.

Vitamin D deficiency is also one of the most common vitamin deficiencies in the developed world today. With the general lack of sunlight and our less varied diets, many foods are beginning to be fortified with vitamin D, but it is still not sufficient. While this deficiency has many potential health risks, Musculoskeletal pain proves to be the most common occurring in nearly 93% of those with low Vitamin D. This form of pain can be quite a burden as it can feel as if all the deep tissue of the body is sore and fatigued. studies thus far have linked deficiency in vitamin D with musculoskeletal pain definitively, and neurons have been found to carry vitamin D receptors. Deficiency can also lead to lower calcium levels and the combination of the two creates a one two punch to later bone health. While a direct mechanism for deficency induced pain has not been previously discovered a recent study provides a likely culprit: sensory hyperinervation.

The recent study by tague et al discovered that vitamin D deficient rats had muscular hyperinervation after only 4 weeks. Muscle strength nor health was significantly altered, neither was overall bone health or skin sensitivity. The only major effects indicated were balance and muscle sensitivity. Previous studies had implicated bone degeneration as a source of pain, however, the administration of excess calcium staved off bone degeneration. This poses the question: how does the lack of vitamin D contribute to this hypersensitivity? The awnser the data indicates is the selective hyperinnervation by putative nociceptors.

Neurons showed to sprout invitro in the absence of 1,25(OH)2D (metabolite of vitamin D). while most neuronal responses are due to the presence of a substrate it appears that VDR acts in response to a lack of substrate as well. VDR regulates PKC, MAPK, PLC, PLA2
, Src, and Raf activation, along with calcium and chloride ion channels. The combination of the alteration in these factors likely induces the axonal growth.

The specificity for Muscles is still odd, as no cutaneous sensitivity or hyperinnervation was detected. This indicates that muscles may be particularly prone to hyperinnervation.

Now that a biological basis for muscular hypersensitivity due to vitamin D deficiency has been established, a likely treatment for muscle pain is obvious: vitamin D supplements. With this information the masses of people suffering from chronic pain may begin to be thinned out, and a distinction between all forms of muscle pain may be made.

Tague et all. Vitamin D Deficiency Promotes Skeletal Muscle
Hypersensitivity and Sensory Hyperinnervation. The Journal of Neuroscience, September 28, 2011. 31(39):13728 ??13738
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Point and Shoot Homicides for The Greater Good

Point and Shoot Homicides for The Greater Good

We buy digital cameras for their ease of use, point and shoot abilities and a variety of preset modes. These familiar settings found on the top of a cameras settings dial allow us to clutter the worlds bandwidth with pictures of ourselves in all sorts of lighting conditions, from beach mode, to the always useful sport mode. Although these preset modes are able to provide us with settings that suit almost every possible environment in which we find the urge to shoot there are times when none of the preset modes seem to do our scene justice. It is at these points that the adventurous will revert to the manual mode offered on many cameras. These manual modes often require planning and significant trial and error - but with enough patience and some luck the possibility for the perfect photo can be achieved in almost every possible situation.

Moral Philosopher and Neuroscientist Joshua Greene at Harvard University, likens these sort of preset and manual modes that we find on our point and shoot cameras, to the ways that humans deal with tough moral dilemmas. In other words when we are presented with a tough moral decision we may react in one of two ways: with an instantaneous emotional response No, I just think thats horrible! (our sport mode) - or via a delayed and obviously pained response that requires us to undergo a sort of cost vs. benefit, utilitarian analysis that serves as our manual mode.

Greene s study sought to find the underlying brain mechanism for these two response types by presenting participants in an fMRI with straight forward questions that required either a: yes, I would do it, or a No, absolutely not! response. Greene monitored the areas of the brain that were activated while participants made their choices as well as the amount of time required for their choice to be made.

The first scenario presented asked participants to imagine a trolley rapidly approaching five workers. You are standing next a to switch that when pulled will divert the trolley subsequently killing one worker while sparing the other five. If you do nothing you essentially allow the five workers to be killed. What was revealed by the fMRI was activation of the participants emotionless and calculating Dorsal Later Prefrontal Cortex (DLPFC) while, the Medial Prefrontal Cortex (MPFC) as well as the Posterior/Cingulate Precuneus, regions associated with emotional cognition, showed relatively low activation. As a result of these activation patterns most participants reasoned that in this very impersonal editing of impending danger, saving 5 vs. 1 was the best choice to be made. The participants were able to separate themselves emotionally from the scenario, i.e. bypassing their emotional preset mode, and instead adopt a calculated manual mode in order to make the utilitarian choice to sacrifice the one for the five.

In the second scenario things become more up close and personal. Participants were asked to imagine that they and another individual, who is wearing a large backpack, are standing on a footbridge over the trolley track. Quickly you realize that pushing the man will stop the trolley (its a really big backpack) before it crushes the five workers, but you will have to push the man off the bridge to his must gruesome death. While the participants decided whether they would push the man or not, the fMRI revealed large amounts of activity not only in the (DLPFC) but as well as the (MPFC), and the Anterior Cingulate Cortex (ACC) which is thought to be used for conflict resolution. What was seen was a considerably longer delay in response times that suggested a large internal conflict within the participants. There seemed to be a disparity between their MPFC providing that initial feelings of repulsion (our emotional preset mode) and the cost/benefit analysis that was undertaken within the DLPFC. Mediating which action would be taken, and contributing to the extension of the response time was the ACC. The results of the scenario are the same, kill one and save five but the methodology differs greatly and as a result most participants agree that they would be incapable of pushing the man and would let the five workers be killed.

Greene reasons that it is our instantaneous and powerful emotional response against the idea of having to physically be involved in the death of someone that allows the emotional MPFC to overpower the logic of the DLPFC contributing to the death of five instead of one. Through enough trials Greene was able to predict based on amount of DLPFC vs. MPFC activation whether the participants would choose to push the man, or take no action and let the five workers be killed.

What Greene suggests from these findings is that we as humans all possess a collection of preset emotional responses to moral situations. Whether they are biological feelings of disgust, or socially influenced learned forms of anxiety that compel us to act in particular situations. These intuitive 'preset' feelings allow us to judge an action such as pushing a man to his death as immoral without much internal deliberation. But when situations are impersonal and do not involve us emotionally we are more readily able to reason our actions and rationalize the sacrifice of one in order to save many we are merely editing the impending danger. But it is when we become personally involved with the situation that we are overpowered by our emotions and deviate from our previous rational decisions, our preset emotional feeling tells us that we cannot author the death of an individual.

Greene argues that although these preset modes, like our camera, equip us with the ability to make the correct moral decision in most normal scenarios, they fail to help us act what some may consider appropriately, when the situations become more complex. He argues that it is in these tough moral dilemmas that we must not revert automatically to our preset emotional responses, but instead we should adopt a rational utilitarian approach that is offered by the manual settings provided by our higher cortical functions.

Many though, are opposed to such a utilitarian view point and argue for a deontological approach that certain moral boundaries ought not be crossed no matter the contribution to the greater good.

So the next time you find yourself in this common trolley dilemma, ask yourself if you will adopt: the easy and quick Sport Mode or whether you will take some more time to fiddle with manual mode to get the best shot.

Greene, Joshua. "The Neural Bases of Cognitive Conflict and Control in Moral Judgment." Neuron 44 (2004): 389-400. SciVerse. Web. 22 Oct. 2011.

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Restoration of Bovine Sanity and a Cure for Neurodegeneration

Mad cow disease. This deadly, presently incurable, brain-eating disease has been the cause of many a steak-lover's trepidation. After all, who wants his brain looking like swiss cheese? It is caused by the consumption or spontaneous generation and accumulation of PrPSc - the misfolded form of cellular prion protein (PrP) - and is responsible for several forms of "swiss cheese brain" besides bovine spongiform encephalopathy (affectionately known as mad cow disease), including the sheep-transmitted scrapie and the human form known as Creutzfeldt-Jakob syndrome, among others. Unfortunately for its victims, PrPSc is much more stable than the properly folded form of the protein and is thus resistant to normal methods of protein digestion (i.e. with protease) and is only known to be degradable via incineration of the infected victim. Clearly, this is an undesirable outcome for the individual who has been unfortunate enough to come into contact with such a protein.

As the misfolded PrPSc aggregates, it forms amyloid fibrils, essentially converting the normally folded PrP to the dark side and eventually causing neuronal cell death and ultimately the death of the organism. However, a recent study of methods to stabilize mouse PrPSc species, published in the Journal of Neuroscience, has shown that prion activity can be reduced by trapping partially digested PrP(27-30) with thienyl pyrimidine compounds.

The process of PrP conversion to the abnormally β-sheet-rich PrPSc form is autocatalytic, that is, it happens spontaneously and independently of other types of molecules. In their study, the researchers discovered that the formation of amyloid fibrils may actually be the "result of a protective process to sequester more dangerous soluble oligomers". As a result, rather than attempting to break the prions apart into smaller, supposedly more easily digested pieces, they decided to attempt to isolate them to avoid increasing the infectivity. Using mouse neuroblastoma cell cultures, they performed various drug assays and blotting techniques, including incubation of fibrils with thienyl pyrimidine compound. When all was said and done, they only observed a minimal decrease in the rate of infectivity, but it was a decrease, nonetheless. They concluded that the binding of thienyl pyrimidine-based drugs diverted dimers and trimers of misfolded protein from their pathological aggregation pathway, trapping them thermodynamically in an energy valley where they could no longer fold into their mortality-causing fibril-forming shape.

Though the study was largely inconclusive, it is clear that meaningful advances were made in discovering that the treatment of prion diseases is not as hopeless as we have believed up to this point. Indeed, the thought of finding a cure seems a daunting task, as the mad cow protein only seems to become more stable under most reaction conditions. However, this study has shown that sometime in the not-so-distant future, the mechanism of misfolding will likely be discovered, a cure for a once incurable disease developed, and we will no longer have to fear prions as much as we have in the past. Also, not only does this research have significant implications for those of us who enjoy a good steak or lamb chop, it may also have far-reaching influence on the treatment of other "prionopathies", including Alzheimer's, Parkinson's and Huntington's Diseases. Since these are diseases which affect a significant fraction of the aging population, research in this vein is critical for the progress of gerontological studies as well.
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Caught in a Lie: The Role of the Brain in Detecting Deception

Vital to everyday social and economic interactions is the ability to accurately discern whether other individuals are being honest or deceitful. While recognizing dishonesty is no easy matter, it is nonetheless possible even in the absence of signals from facial expression, through careful attention to nonverbal cues. Researcher Julie Grèzes and her colleagues have identified the brain mechanisms that underlie detection of deceptive intent through the use of fMRI technology.

The study involved imaging 11 participants as they viewed videos of actors with blurred faces lifting boxes, and evaluated whether the actors were attempting to deceive them regarding the weight of the box. The results from this experiment were compared to the results from a previous study in which participants were asked to judge whether actors' expectations of a box's weight were false. The key contrasting variable was the judgment of of deceptive intent in the current study, versus the judgment of a false belief resulting in accidental deception in the previous study.

Their research concluded that the amygdala and rostral anterior cingulate cortex were both significantly activated when the participants judged the actors as being intentionally deceptive, yet not when the actors were judged to have unknowingly erroneous beliefs that led to accidental deception.

The amygdala is known to be a critical aspect of the neural circuitry concerning emotion and value appraisal. Additionally, the anterior cingulate cortex is activated when there is intent to directly communicate with the participant, indicated by eye contact and use of the participant's name. Based on such, the researchers speculate that activation of the amygdala and anterior cingulate cortex may be suggestive of the observers' valuation of social intentions towards themselves, and could thereby reflect an emotional response to being misled.

Whether activated by an internal sense of fairness or rather an assessment of social intention, the amygdala and rostral anterior cingulate cortex are working together to help catch liars everywhere, red handed.

The original paper can be viewed at:
Posted by      Anjali C. at 12:00 AM MDT
  Gino Ciarroni  says:
Interesting Anjali,
I find this article to be very intuitive. I question if the concept of deception is an evolved basic instinct. The Amygdala and and rostral anterior cingulate cortex both are triggered in basic survival based learning. The dorsal and rostral areas of the ACC both seem to be affected by rewards and losses associated with errors. The rostral ACC seems to be active after an error commission, indicating an error response function.

While the Amygdala, as part of the limbic system, deals with emotional learing, memory modulation, and social interaction. In regards to social interaction, The amygdala volume correlates positively with both the size (the number of contacts a person has) and the complexity (the number of different groups to which a person belongs) of social networks. Individuals with larger amygdalae had larger and more complex social networks. These people were also better able to make accurate social judgments about other persons' faces. It is hypothesized that larger amygdalae allow for greater emotional intelligence, enabling greater societal integration and cooperation with others. Can Deception be a survival interpretation of where or not we see a stimuli/person as threatening or benefiting? I wonder using the basic parameters, if animals can detect deception.

The amygdala processes reactions to violations concerning personal space. These reactions are absent in persons in whom the amygdala is damaged bilaterally.[42] Furthermore, the amygdala is found to be activated in fMRI when people observe that others are physically close to them, such as when a person being scanned knows that an experimenter is standing immediately next to the scanner, versus standing at a distance
Posted on Fri, 28 Oct 2011 12:02 PM MDT by Gino C.
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October 23, 2011

To sleep or not to sleep

We've all been told that sleep has benefits, especially in college where sleep becomes more of a luxury than anything else. Sometimes there is just not enough time, but more often than not we are unwilling to give up the things we love just to have two more hours of sleep. But nonetheless I think it's safe to say that we have all experienced benefits from a good nights sleep. We need that extra energy so that the next day can suck it right out again. But why is it that we feel rested after sleeping for a decent amount of time?
Scientists have been trying to answer this question for a long time and from various angles. More recently researchers have suggested that a difference in the brain's ATP level might be linked to this phenomena. It's an interesting thought since ATP is the energy source of the body. But why the brain?
The brain only encompasses about 2% of our entire body mass. However it is one of the prime energy users. The brain utilizes about 20% of glucose and oxygen, both prime energy sources for the body. That means that 1/5 of the energy is being used by an organ that only comprises 2% of the body. So it does make sense to take a closer look at the brain when it comes to ATP levels.
A recent study published in the Journal of Neuroscience has shown that there are indeed differences in ATP levels during not only awake and sleep states but also the different sleep states and different brain areas. The results showed an ATP surge during the sleep state occurring at the onset hours of sleep.
So what does this surge do? Sadly enough it doesn't magically provide extra information for the next days exam, though that would be nice. The surge serves as nourishment to our brain, so that biosynthetic pathways can be restored. So in a way these surges of ATP are little helpers.
While working on this research, the researchers discovered that the ATP surges showed a correlation to the EEG NREM delta activity in spontaneous sleep. EEG NREM delta activity simply means that the waves generated by the NREM sleep period were of size delta and measured by an EEG. In the NREM period the neuronal activity drops and less energy is consumed which is exactly when the surge of ATP would occur.
Now how is this helpful to us other than just having gained some extra knowledge? The research shows the importance of sleep to our bodies' homeostasis. During the day we (hopefully) have high neural activity thus we are using up a lot of energy/ATP, but during the night we have low neural activity and thus use up less energy. So we get an energy surge at the onset of our sleep to take care of the restoration of biosynthetic pathways; at this point it is important that we are not using that energy surge for other purposes (like neural activity). So if we wake up to early because class might just be about to start, we have not been able to fully restore the biosynthetical pathways before our neural activity sets in again.
So you might argue that sleep is an important factor in test preparation as well. You might have studied as well as possible but if you did not let your body do its work over night, your biosynthetical pathways are not up to date.
So be kind and give your body a decent amount of sleep, that way you only have to worry about the actual studying.

Full article:
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Can You Fool Yourself Out Of Depression?

Major depression has long been a disorder weighing down on its victims, but fascinating neuroscientists. Can we use the placebo effect to leave the confines of a depressed world? What exactly lies behind the mechanisms of the placebo analgesic effect? To find out, researchers compared the effect of fluoxetine and a placebo and using neural imaging techniques, compared which regions of the brain showed activity/change at the beginning of the study, at six weeks, and at the end. What they found was that each treatment method caused an increase in activity in the prefrontal and posterior cingulate and decreases in subgenual cingulate. Fluoxetine worked better, and the results of the placebo were inconclusive. Although not tested in an extended study, researchers also compared the effect of various psychotherapies as opposed to placebos and found that they each affected different regions of the brain and that, unfortunately the placebo effect only worked for a little while.

But hold up! If our emotions are strictly based on the balance of chemicals in our brain, then how could we possibly fool ourselves of how we really feel even for a second? The placebo analgesic effect is when our brains signal to generate endorphins in order to alleviate pain.

The expectation of getting better plays a huge role in how well the placebo effect works and the way this is tested is through the use a drug called naloxone. Naloxone counters the effect of opioids and is used to reverse heroin/morphine overdoses in modern clinical practice. It was found that in patients where the placebo analgesic was brought on by strong expectations, the response could be blocked by naloxone. However, if the expectation cues were decreased, naloxone would not work. This concludes that in order for naloxone to work, there needs to be a large amount of endogenous opioid concentration.
Let�??s delve into this a little further. If the patients were exposed to various opioid drugs, the placebo effect could be reversed by naloxone, but if they were not, they were insensitive to naloxone. It can be concluded that naloxone only works in certain physiological conditions.

A typical side effect of opioids is respiratory depression. It was hypothesized that a placebo could mimic the effects of a drug which causes mild respiratory depression. Repeated injections of buprenorphine during the study and then a final injection of a placebo showed that the placebo was able to induce respiratory depression in the same way that the opioid did.

Placebo analgesics only work on certain people and in certain physiological conditions. But we know that they can induce extreme physiological changes, for the better or worse. Further studies need to be conducted to prove how exactly our brain can practice �??mind over matter�??.

all info was taken from
Posted by      Dora P. at 11:55 PM MDT
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  Emily Nelson  says:
Personally, I don't believe that anyone can fool himself out of depression. It will only make things worse if you won't acknowledge the fact that you are depressed. Seeking help is one of the best things to do to combat depression as well as meditation. having someone to talk to can make a huge difference. TEDx speaker Sydney
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In the eye of the beholder

Optic illusions are fascinating. Sparking curiosity, intrigue and doubt in minds gazing at the impossibilities spawned by them. Most people have been exposed to a variation of the famous "which object is bigger" illusion. If you don't know what I'm talking about, there are two objects of equal size physically, surrounded by various contextual components. These various components give the viewer a false sense of subjectivity in which one object appears larger than the other, even though both objects are identical. It turns out neuroscientists want to better understand the cause behind these false perceptions and even predict human subjectivity in object size.

Your brain contains a primary visual cortex, let's call this thing V1. The size and surface area of V1 has a large range of variability from person to person. Scientists have correlated the surface area of V1 to the subjectivity in object size. Experimentation took place during September 2010 with 30 subjects with the hypothesize correlating V1 surface area and conscious perception differences via FMRI technology. Subjects viewed a "Ebbinghaus" illusion as well as a "Ponzo" illusion. Both are forms of physically identical objects appearing different sizes due to contextual differences surrounding the objects. The Ebbinghaus illusion appears larger due to different size circles surrounding the center circle. While the Ponzo illusion appears larger due to the 3-D context surrounding the images. The resulting data showed a strong and negative correlation between V1 surface area and subjective object size. Meaning: The less V1 surface area, the bigger the difference between the identical objects perceived by subjects. It should be noted that the Ebbinghaus illusion yielded better data for relation than the Ponzo illusion. "The ability to judge fine visual differences in physical stimuli (Vernier acuity) is correlated with the degree of cortical magnification in primary visual cortex".

The article also addressed V1 surface area and brain size do not have a direct relationship. Meaning a bigger brain doesn't constitute greater V1 surface area. Therefore having a larger brain doesn't mean a person is better at correctly determining visual stimuli. V1 actually tended to be smaller in larger brains.

Consider the possibilities of predicting human behavior, opinions and subjectivities by knowing who is more susceptible to illusions and visual stimuli based on brain structure. Knowing exactly how well people can perform certain tasks depending on their brain structure may be far off in the future but it's roots seem to have a firm plantation in the field of research.

Most people like to believe they are in total control of their thoughts, subjectivities and opinions. Yet in this experiment, it showed that people having less surface area of the V1, perceptions of object size were distorted. Your perspective and opinions may not be as genuine as you original believed them to be. Rather just by products of the human brain analyzing stimuli. As neuroscience continues to unravel the mysteries of the human mind ideas such as free will, consciousness and perception may need to be redefined.

(All information was taken from
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Depressed due to stress? Blame your genes...

Everyone experiences stress on a daily basis, whether it be due to misplaced car keys or the impending doom of taking Intro to Neuroscience quizzes online, knowing that Teamviewer will crash at least 3 times. There are many ways to deal with everyday stress; some combat the stressor head on, and others try finding ways around it. Us college students seem to combat the never-ending stress during the week with shots (usually one too many) on weekend nights. Most of us can find ways to effectively relieve this everyday stress and continue on our merry ways, ready for the next stressor that rears its ugly head. But for some, stress can cause a detour from this merry path, instead leading to a path of anhedonia, a defining symptom of depression characterized by an inability to find pleasure in activities once found pleasurable. So why can most people cope with stress, while others seem to fall apart at the seams? Ryan Bogdan and his affiliates may have found a simple answer as to why some follow this crippling detour.

Before I go any further, let me give some background into the neurobiology of stress response. Corticotropin-releasing hormone (CRH) is a hormone released by the paraventricular nucleus of the hypothalamus in response to stressful stimuli. CRH binds to the corticotropin-releasing hormone type 1 receptor (CRHR1) to exert its critical role in the regulation of the hypothalamic-pituitary-adrenal (HPA) axis, a complex neuronal network responsible for a wide variety of processes, including mood and reactions to stress. Got all that? Good.

Recently discovered is a genetic variation in the DNA encoding CRHR1, coined the CRHR1 A allele, that contains a single point mutation. This small mutation has big consequences, most notably an attenuated response to positive feedback in the ventral striatal region under stress. So what the hell does this all mean? Simply put, it means that the A allele of this receptor have disrupts processing rewarding stimuli under stress. When an individual cannot process something as rewarding, such as activities and hobbies that they used to find pleasurable (anhedonia), the inevitable result is clinical depression.

Ryan Bogdan used this information collected on the A allele to design a study focused on reward learning, an important behavioral aspect of anhedonia. In this study, control subjects and subjects homozygous for the A allele were subjected to two separate tasks involving reward; one task was stress-free, the other under the stressful possibility of electric shock should one fail the task. Under the stress condition, subjects homozygous for the A allele performed far more poorly than the control subjects, confirming that this genetic mutation produced stress-induced behavioral deficits in reward learning. Surprisingly, these same A allele subjects performed better than control under the no-stress condition.

This unfortunate genotype sheds more light on the high cormobidity between stress, anxiety, and depression. However, it could also possibly lead to effective treatments for families carrying this A allele. Stress sucks for everyone, but for certain individuals, it sucks way, way worse. Keep this in mind while studying for your next midterm, and remember, the weekend (and shots) are coming soon.
Posted by      Kevin K. at 11:27 PM MDT
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Edited by      Justin E. at 11:26 PM MDT
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As I was trying to post I kept getting messages indicating that my blog had failed to post, so I kept changing small things and seeing if it would post after these changes. It lied to me, though. It was posting the whole time so now there are lots of posts that I can't delete. Sorry for that.
Posted on Mon, 24 Oct 2011 12:11 AM MDT by Justin E.

Refrigerator + Toaster = Kitchen: The algebra of familiarity

When it comes to recognizing visual settings, we humans are pretty darn adept. We can immediately distinguish the difference between say, our comfortable bedrooms and a busy intersection in no time at all. Good thing, too, or else we'd often find ourselves in rather sticky situations. But what allows us to differentiate between the various settings we daily find ourselves in? It turns out that it all boils down to some simple math involving objects that we're all too familiar with. Without having to analyze the entire scene, our brains can recognize a traffic light and crosswalk, for instance, and associate these objects with the environment we most often see them in, an intersection. This new line of thinking was proposed in a recent paper published in Nature Neuroscience by MacEvoy and Epstein.

Now, the math seems pretty black and white, right? A toilet plus a bathtub must equal a bathroom and a bed plus a closet full of clothing definitely must mean that we're in a bedroom. However, there are shades of gray. For instance, where does a chair belong? Unlike the previous examples, it's a lot harder to only associate a chair with one specific scene, but that's where our brain's awesome processing power comes in. While we process the chair, we're also processing a multitude of other objects in the setting and combining their meanings into a much more specific setting than the one we'd be able to associate with a chair alone.

Now, to some of you this may seem rather intuitive, but MacEvoy and Epstein were able to support this claim with one of the most valuable things to neuroscientists and to scientists in general: cold, hard data. By using fMRI the duo measured the brain activity of their participants while showing them pictures of four types of scenes: an intersection, a bathroom, a kitchen, and a playground. By comparing the brain's responses to the scenes and to familiar objects it was found that the responses to an individual item were almost identical to the responses that the participant had to an entire scene. For example, the brain patterns elicited by a toilet were incredibly similar to those provoked by an entire bathroom. These responses were also found to be localized to the lateral occipital cortex, or LOC. The parahippocampal place area (PPA), a region that has been proposed to be involved in scene recognition, didn't form these types of individual objects-to-generalized scene associations. This seems to support the idea that the PPA is involved with more large-scale scene recognition (such as a baseball stadium or warehouse), where the scene's spatial layout is useful for identification. However, scientists are not entirely sure of how these two areas work together.

So, the next time you find yourself in a familiar setting it might be a good idea to stop and wonder what objects led you to that familiar feeling and maybe to give your brain a little credit for its amazing capacity to recognize your surroundings.

The original paper can be found at:
Edited by      Justin E. at 11:30 PM MDT
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The Urge to Experience, How We Respond to Novelty

Human beings once were localized to a a few locations on earth, and yet over time they explored and expanded. The need to travel and experience new areas and landscapes and discover new worlds is what led the polynesians to discover all the islands in the south pacific, Columbus to the new world, and Niel Armstrong to our own moon, and that same desire to experience the unknown is the topic of interest in Brian Knutson's and Jeffrey C. Cooper's article The Lure of the Unknown in the 51 volume, issue 3 of the August 3 2006 copy of the Neuron.

Before this study, the Ventral Tegmental Area and the Substantia Nigra were heavily implicated in the process of conferring salience onto a stimuli. For the purpose of this experiment, the researchers defined salience as one of 4 different pictures presented. One set of pictures depicted novel scenes, one set showed negative scenes, one set was behavioral in nature, as when showed the picture the subjects then were expected to perform a simple action, and one set were simply neutral, and repeated for the last portion of the experiment. These different pictures represented the different forms of salience that could be conferred onto such stimuli. It turns out that the novel pictures through use of fMRI showed the most activity in the VTA and SN, as well as portions of the striatum and the hippocampus, implicating that we place the most salience onto novel pictures and stimuli as opposed to others. Other pictures then showed increased activity in different regions of the brain, such as the negative stimulus activating the locus coeruleus and the amygdala while the neutral pictures activating the hippocampus and the anterior cingulate.

The question of memory stimulation was raised, and contrary to the prediction made due to the fact that the hippocampus was stimulated by novel pictures, memory of novel pictures was not higher than that of repeated pictures. However, an interesting outcome of a related study showed that repeated pictures with the prescence of a few novel pictures thrown in were granted a temporary memory boost, undetectable 1 day later but present after 20 minutes. This contrasted with studies showing that stimuli coupled with reward cues also received memory enhancements implies the possibility that novel stimuli elicit a reward response throughout the brain. Unfortunately the study did not have a category designated for positive pictures which could have played the role as the reward response and then compared to the novel pictures to look for any similarities in the response of the VTA and the SN, as well as the effect it has on memory to see whether novel pictures play reward roles.

These studies collectively form a new basis for further study into the human response to novelty, potentially discovering whether we gain a reward sensation from novelty and whether that even makes us go in search of it, just as historical examples such as Galileo and Niel Armstrong would seem to suggest in their descriptions of experiencing the novelties of space and the limits of the world.

Full Article:
Posted by      Christopher R. at 11:22 PM MDT
Tags: amygdala, fmri, memory
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The Neuroanatomy Behind Sociability

The Neuroanatomy Behind Sociability

People, like all primates, are inherently social animals. We live, work, and play together. We are defined by our relationships. However, individuals have varying degrees of sociability. The size and shape of our social networks varies from person to person. There are social butterflies - people who seem to know someone wherever they go. Who boast large numbers of contacts and network effortlessly. On the other end of the spectrum, there are the wallflowers - those with more modest social networks, who interact mainly with a select handful of people. A person's sociability - whether they are a social butterfly, or a wallflower, or somewhere in between - seems innate. It seems to be a fundamental characteristic of a person.

As a strong introvert, I've often wondered, what makes one person a social butterfly and another a wallflower? What's the difference between a person with 5 friends and person with 50?

According to an article published in the journal Nature Neuroscience in February, the answer lies in part with the Amygdala. Researchers took 58 healthy men and women ages 19 to 83 and measured both the size and complexity of the subjects' social networks using something called the Social Network Index. The results of the analysis were then compared with the relative size of the subjects' amygdalas. There was significant correlation. The authors state,

"We found that amygdala volume correlates with the size and complexity of social networks in adult humans. An exploratory analysis of subcortical structures did not find strong evidence for similar relationships with any other structure, but there were associations between social network variables and cortical thickness in three cortical areas, two of them with amygdala connectivity. These findings indicate that the amygdala is important in social behavior."

In addition, while amygdala volume was found to be correlated specifically with social network size, "amygdala volume did not relate to other measures of social functioning such as perceived social support and life satisfaction." This is important because it means that the findings of correlation are more specific than social functioning as a whole.

These results were not entirely surprising to the researchers. Previous studies in other (nonhuman) primates "strongly support a link between amygdala volume and social network size and social behavior." This latest research is, however, the first study to show correlation within a certain species and between individuals of that species.

So, does this mean that a person's social fate is sealed? That their social network size was dictated at conception along with eye color? Luckily, the answer is no; at least not entirely. Within the study, there were individuals with small amygdalas and enviable social networks as well as individuals with larger amygdalas, yet smaller network sizes. In addition, the results are corollary, and say nothing about social learning or nurture (as opposed to nature). (So, those Dale Carnegie books might prove useful yet!)

The authors' analysis of the study does not seem very focused on the individual. The important thing appears to be the trend - the statistical correlation. The authors hold that the findings are important because they support an evolutionary view called the 'social brain hypothesis'. The social brain hypothesis states that mammals evolved larger brains in part as a response to selective pressures to be more social, which required greater processing capacity. The authors also expect these results to act as preliminary data in future studies looking at larger brain networks that dictate social network size and complexity.

In spite of these more lofty applications, the individual correlation still remains. So, the next time you assess your Facebook friend quota, whether its admirable, or not so much, remember, it might simply reflect your respective amygdala.
Posted by      Kyle K. at 11:16 PM MDT
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Recreational drugs: who doesn't want to know? Case file on MDMA

How does it work? What are the physiological effects of this ??rave?? drug? What are the long lasting consequences? Addiction, irreversible damage or is it safe for use? What can we learn from the mechanisms of MDMA on our brains?
To answer these questions we must understand it's mechanism on a molecular stand point. MDMA preferentially binds to serotonin transporters (SERT) on the presynaptic membrane. This causes an increase in the neurotransmitter serotonin (5-HT) in the synapse. MDMA does so by blocking 5-HT from binding SERT, thus impeding 5-HT uptake. Also, MDMA reverses SERT function: instead SERT allows MDMA into the pretsynaptic neuron while allowing 5-HT out of cell and into the cleft. Finally, 5-HT levels are increased when MDMA within the presynaptic cell invades 5-HT storage vesicles allowing 5-HT to exit trough the nerve cell membrane. To better visualize the process the following has a schematic depiction from 2:39 to 2:56 major increases in serotonin levels cause an increased firing of serotonergic neurons translated by physiological effects including mood elevation, increased sociability and hyperlocomotion. Note that a similar mechanism for dopamine (DA) release is observed but to a lesser degree then 5-HT release.

To further understand the effects of MDMA researchers at l'Universite Pierre et Marie Curie in Paris, France took interest in the role of 5-HT2B receptor in MDMA evoked hyperactivity. You might wonder:Why look at this particular 5-HT receptor? First , because it has been shown that it governs 5-HT transport by increasing phosphorylation of SERT. This promotes SERT activation in raphe nuclei where raphe neurons are the principal source of 5-HT release. This indicates a regulatory role of 5-HT2B in 5-HT release. Also, MDMA +MDA metabolite bind and activate 5-HT2B in particular, at the same levels seen during first use. Furthermore, MDMA +MDA elicit prolonged mitogenic responses in certain cells by directly activating specifically 5-HT2B and no other 5-HT receptor.

The challenge in investigating the role of a particular 5-HT receptor is distinguishing it from other 5-HT receptors. In order to do this two methods were utilized: a pharmacological approach using a 5-HT2B antagonist ( RS127445 which is 1000 fold selective for 5-HT2B vs. other 5-HT receptors, SERT or DAT (DA transporter) ) and a genetic approach knocking out 5-HT2B genes and thus 5-HT2B expression.

Behavioral data was established by measurement of locomotion, using the number of times mice subjects passed through lasers installed within a tunnel. Wild type (WT, with 5-HT2B) mice injected with MDMA showed hyperlocomotion relative to WT mice injected with saline. And WT mice injected with MDMA and 0.1 mg/kg RS127445 antagonist or more showed no hyperlocomotion and similar motion to WT mice injected with just saline. Note that RS127445 has no effect on baseline locomotion. Similar results were obtained when -/- 5-HT2B mice were used i.e. MDMA did not cause hyperlocomotion in these mice without 5-HT2B receptors. These results show 5-HT2B is necessary for MDMA induced hyperlocomotion.

The molecular phenomenon of 5-HT and DA release causing hyperactivity is observed in the ventral tegmental area (VTA) and nucleus accumbens (NAcc). WT/saline vs. WT/MDMA showed an 80 fold increase in 70 min for 5-HT and an 80 fold increase in 50 min for DA in both VTA+ NAcc. Also, WT/saline vs. WT/MDMA+RS127445 showed no significant difference respectively in both areas or against each other in DA and 5-HT concentrations. Finally, there was no significant difference between -/- 5-HT2B/saline and -/-5-HT2B/MDMA in NAcc. These results show the psychomotor stimulant effect of MDMA is subsequent to an increase in 5-HT and DA realese in the VTA + Nacc which is 5-HT2B dependent.

Now lets not forget that MDMA binds SERT and DAT, regulated by 5-HT2B. For the previous results to be conclusive SERT and DAT levels and their functionality must be constant across all of the experiments for WT and -/-5-HT2B mice. SERT and DAT expression was quantified by introducing specific ligands and observing their radioactive expression at different concentrations of 5-HT and DA respectively. Amounts of SERT and DAT were the same for both WT and -/- 5-HT2B mice. Functionality was observed using the same ligand-markers and their uptake by synaptosomes in function of 5-HT and DA concentrations. Again, functionality was conserved for both transporters in WT and -/-5HT2B mice.

The totality of these observations lead to the conclusion that 5-HT2B acts presynaptically in raphe neurons to permit MDMA induced SERT dependent 5-HT release. This is further verified by the presence of 5HT2B protein and SERT in raphe nuclei and the quantity of functional 5HT2B, which is sufficient to effect 5-HT concentrations, in vivo. The consequent 5-HT release can be observed in vitro in a serotoninergic nerve ending. The final conclusion seems to correlate with the fact that NAcc and VTA ascending serotoninergic projections arise from the raphe nuclei.

The intense search to understand the underlying mechanism used by MDMA gives us clues as to the functioning of neurophysiological pathways. For example, the knowledge that 5-HT2B plays a role in locomotion may be of utility in physical rehabilitation or in cases where even baseline movement isn't observed. Also the fact that 5-HT2B levels are found at the same level as during a first recreational use indicates a change in synaptic morphology translated by an increased tolerance to 5-HT release. That is even after just one dose, it is harder to obtain the euphoric effects (which ??ravers?? search for when taking MDMA) without the drug and continually need to increase the dosage in order to find the ??high??. However, MDMA has not been shown to be physically addictive and the only addiction is one associated to the emotional state reached when taking the ??Love Drug??. Use of MDMA depends on a personal perspective of risk and reward, like so many other things in life!

All information was taken from:

Recreational drugs: who doesn't want to know? Case file on MDMA

How does it work? What are the physiological effects of this ??rave?? drug? What are the long lasting consequences? Addiction, irreversible damage or is it safe for use? What can we learn from the mechanisms of MDMA on our brains?
To answer these questions we must understand it's mechanism on a molecular stand point. MDMA preferentially binds to serotonin transporters (SERT) on the presynaptic membrane. This causes an increase in the neurotransmitter serotonin (5-HT) in the synapse. MDMA does so by blocking 5-HT from binding SERT, thus impeding 5-HT uptake. Also, MDMA reverses SERT function: instead SERT allows MDMA into the pretsynaptic neuron while allowing 5-HT out of cell and into the cleft. Finally, 5-HT levels are increased when MDMA within the presynaptic cell invades 5-HT storage vesicles allowing 5-HT to exit trough the nerve cell membrane. To better visualize the process the following has a schematic depiction from 2:39 to 2:56 major increases in serotonin levels cause an increased firing of serotonergic neurons translated by physiological effects including mood elevation, increased sociability and hyperlocomotion. Note that a similar mechanism for dopamine (DA) release is observed but to a lesser degree then 5-HT release.

To further understand the effects of MDMA researchers at l'Universite Pierre et Marie Curie in Paris, France took interest in the role of 5-HT2B receptor in MDMA evoked hyperactivity. You might wonder:Why look at this particular 5-HT receptor? First , because it has been shown that it governs 5-HT transport by increasing phosphorylation of SERT. This promotes SERT activation in raphe nuclei where raphe neurons are the principal source of 5-HT release. This indicates a regulatory role of 5-HT2B in 5-HT release. Also, MDMA +MDA metabolite bind and activate 5-HT2B in particular, at the same levels seen during first use. Furthermore, MDMA +MDA elicit prolonged mitogenic responses in certain cells by directly activating specifically 5-HT2B and no other 5-HT receptor.

The challenge in investigating the role of a particular 5-HT receptor is distinguishing it from other 5-HT receptors. In order to do this two methods were utilized: a pharmacological approach using a 5-HT2B antagonist ( RS127445 which is 1000 fold selective for 5-HT2B vs. other 5-HT receptors, SERT or DAT (DA transporter) ) and a genetic approach knocking out 5-HT2B genes and thus 5-HT2B expression.

Behavioral data was established by measurement of locomotion, using the number of times mice subjects passed through lasers installed within a tunnel. Wild type (WT, with 5-HT2B) mice injected with MDMA showed hyperlocomotion relative to WT mice injected with saline. And WT mice injected with MDMA and 0.1 mg/kg RS127445 antagonist or more showed no hyperlocomotion and similar motion to WT mice injected with just saline. Note that RS127445 has no effect on baseline locomotion. Similar results were obtained when -/- 5-HT2B mice were used i.e. MDMA did not cause hyperlocomotion in these mice without 5-HT2B receptors. These results show 5-HT2B is necessary for MDMA induced hyperlocomotion.

The molecular phenomenon of 5-HT and DA release causing hyperactivity is observed in the ventral tegmental area (VTA) and nucleus accumbens (NAcc). WT/saline vs. WT/MDMA showed an 80 fold increase in 70 min for 5-HT and an 80 fold increase in 50 min for DA in both VTA+ NAcc. Also, WT/saline vs. WT/MDMA+RS127445 showed no significant difference respectively in both areas or against each other in DA and 5-HT concentrations. Finally, there was no significant difference between -/- 5-HT2B/saline and -/-5-HT2B/MDMA in NAcc. These results show the psychomotor stimulant effect of MDMA is subsequent to an increase in 5-HT and DA realese in the VTA + Nacc which is 5-HT2B dependent.

Now lets not forget that MDMA binds SERT and DAT, regulated by 5-HT2B. For the previous results to be conclusive SERT and DAT levels and their functionality must be constant across all of the experiments for WT and -/-5-HT2B mice. SERT and DAT expression was quantified by introducing specific ligands and observing their radioactive expression at different concentrations of 5-HT and DA respectively. Amounts of SERT and DAT were the same for both WT and -/- 5-HT2B mice. Functionality was observed using the same ligand-markers and their uptake by synaptosomes in function of 5-HT and DA concentrations. Again, functionality was conserved for both transporters in WT and -/-5HT2B mice.

The totality of these observations lead to the conclusion that 5-HT2B acts presynaptically in raphe neurons to permit MDMA induced SERT dependent 5-HT release. This is further verified by the presence of 5HT2B protein and SERT in raphe nuclei and the quantity of functional 5HT2B, which is sufficient to effect 5-HT concentrations, in vivo. The consequent 5-HT release can be observed in vitro in a serotoninergic nerve ending. The final conclusion seems to correlate with the fact that NAcc and VTA ascending serotoninergic projections arise from the raphe nuclei.

The intense search to understand the underlying mechanism used by MDMA gives us clues as to the functioning of neurophysiological pathways. For example, the knowledge that 5-HT2B plays a role in locomotion may be of utility in physical rehabilitation or in cases where even baseline movement isn't observed. Also the fact that 5-HT2B levels are found at the same level as during a first recreational use indicates a change in synaptic morphology translated by an increased tolerance to 5-HT release. That is even after just one dose, it is harder to obtain the euphoric effects (which ??ravers?? search for when taking MDMA) without the drug and continually need to increase the dosage in order to find the ??high??. However, MDMA has not been shown to be physically addictive and the only addiction is one associated to the emotional state reached when taking the ??Love Drug??. Use of MDMA depends on a personal perspective of risk and reward, like so many other things in life!

All information was taken from:

Recreational drugs: who doesn't want to know? Case file on MDMA

How does it work? What are the physiological effects of this ??rave?? drug? What are the long lasting consequences? Addiction, irreversible damage or is it safe for use? What can we learn from the mechanisms of MDMA on our brains?
To answer these questions we must understand it's mechanism on a molecular stand point. MDMA preferentially binds to serotonin transporters (SERT) on the presynaptic membrane. This causes an increase in the neurotransmitter serotonin (5-HT) in the synapse. MDMA does so by blocking 5-HT from binding SERT, thus impeding 5-HT uptake. Also, MDMA reverses SERT function: instead SERT allows MDMA into the pretsynaptic neuron while allowing 5-HT out of cell and into the cleft. Finally, 5-HT levels are increased when MDMA within the presynaptic cell invades 5-HT storage vesicles allowing 5-HT to exit trough the nerve cell membrane. To better visualize the process the following has a schematic depiction from 2:39 to 2:56 major increases in serotonin levels cause an increased firing of serotonergic neurons translated by physiological effects including mood elevation, increased sociability and hyperlocomotion. Note that a similar mechanism for dopamine (DA) release is observed but to a lesser degree then 5-HT release.

To further understand the effects of MDMA researchers at l'Universite Pierre et Marie Curie in Paris, France took interest in the role of 5-HT2B receptor in MDMA evoked hyperactivity. You might wonder:Why look at this particular 5-HT receptor? First , because it has been shown that it governs 5-HT transport by increasing phosphorylation of SERT. This promotes SERT activation in raphe nuclei where raphe neurons are the principal source of 5-HT release. This indicates a regulatory role of 5-HT2B in 5-HT release. Also, MDMA +MDA metabolite bind and activate 5-HT2B in particular, at the same levels seen during first use. Furthermore, MDMA +MDA elicit prolonged mitogenic responses in certain cells by directly activating specifically 5-HT2B and no other 5-HT receptor.

The challenge in investigating the role of a particular 5-HT receptor is distinguishing it from other 5-HT receptors. In order to do this two methods were utilized: a pharmacological approach using a 5-HT2B antagonist ( RS127445 which is 1000 fold selective for 5-HT2B vs. other 5-HT receptors, SERT or DAT (DA transporter) ) and a genetic approach knocking out 5-HT2B genes and thus 5-HT2B expression.

Behavioral data was established by measurement of locomotion, using the number of times mice subjects passed through lasers installed within a tunnel. Wild type (WT, with 5-HT2B) mice injected with MDMA showed hyperlocomotion relative to WT mice injected with saline. And WT mice injected with MDMA and 0.1 mg/kg RS127445 antagonist or more showed no hyperlocomotion and similar motion to WT mice injected with just saline. Note that RS127445 has no effect on baseline locomotion. Similar results were obtained when -/- 5-HT2B mice were used i.e. MDMA did not cause hyperlocomotion in these mice without 5-HT2B receptors. These results show 5-HT2B is necessary for MDMA induced hyperlocomotion.

The molecular phenomenon of 5-HT and DA release causing hyperactivity is observed in the ventral tegmental area (VTA) and nucleus accumbens (NAcc). WT/saline vs. WT/MDMA showed an 80 fold increase in 70 min for 5-HT and an 80 fold increase in 50 min for DA in both VTA+ NAcc. Also, WT/saline vs. WT/MDMA+RS127445 showed no significant difference respectively in both areas or against each other in DA and 5-HT concentrations. Finally, there was no significant difference between -/- 5-HT2B/saline and -/-5-HT2B/MDMA in NAcc. These results show the psychomotor stimulant effect of MDMA is subsequent to an increase in 5-HT and DA realese in the VTA + Nacc which is 5-HT2B dependent.

Now lets not forget that MDMA binds SERT and DAT, regulated by 5-HT2B. For the previous results to be conclusive SERT and DAT levels and their functionality must be constant across all of the experiments for WT and -/-5-HT2B mice. SERT and DAT expression was quantified by introducing specific ligands and observing their radioactive expression at different concentrations of 5-HT and DA respectively. Amounts of SERT and DAT were the same for both WT and -/- 5-HT2B mice. Functionality was observed using the same ligand-markers and their uptake by synaptosomes in function of 5-HT and DA concentrations. Again, functionality was conserved for both transporters in WT and -/-5HT2B mice.

The totality of these observations lead to the conclusion that 5-HT2B acts presynaptically in raphe neurons to permit MDMA induced SERT dependent 5-HT release. This is further verified by the presence of 5HT2B protein and SERT in raphe nuclei and the quantity of functional 5HT2B, which is sufficient to effect 5-HT concentrations, in vivo. The consequent 5-HT release can be observed in vitro in a serotoninergic nerve ending. The final conclusion seems to correlate with the fact that NAcc and VTA ascending serotoninergic projections arise from the raphe nuclei.

The intense search to understand the underlying mechanism used by MDMA gives us clues as to the functioning of neurophysiological pathways. For example, the knowledge that 5-HT2B plays a role in locomotion may be of utility in physical rehabilitation or in cases where even baseline movement isn't observed. Also the fact that 5-HT2B levels are found at the same level as during a first recreational use indicates a change in synaptic morphology translated by an increased tolerance to 5-HT release. That is even after just one dose, it is harder to obtain the euphoric effects (which ??ravers?? search for when taking MDMA) without the drug and continually need to increase the dosage in order to find the ??high??. However, MDMA has not been shown to be physically addictive and the only addiction is one associated to the emotional state reached when taking the ??Love Drug??. Use of MDMA depends on a personal perspective of risk and reward, like so many other things in life!

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  charlly korpa  says:
This post is including all the information about MDMA, the recreational drug. There are many other dangerous recreational drugs. And the first place occurs the MDMA. automatic gate installation I got the complete details of the effects of MDMA from this post.
Posted on Sun, 24 May 2020 11:47 PM MDT by charlly k.
  Emily Nelson  says:
Good read! Recreational drugs have been illegal in some cities and countries. Over the years, it has been a debate among politicians and yet, there have been different opinions on it. For some, it's their way of escaping from reality, though. book a speaker sydney
Posted on Wed, 27 May 2020 4:56 AM MDT by Emily N.
  Chloe Summers  says:
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Plugged In: The Brain-Computer Interface

Imagine playing your favorite video game and controlling it just through thought. Sounds impossible right? Actually this technology already exists and is currently being used for therapeutic purposes. This amazing technology is called neurofeedback. It works by measuring an individual's brain waves at different states of being through the use of an EEG and then trains the brain to emulate those waves present in the desired state of the individual.

However this technology is very specific to each individual due to the fact that different people engage in different areas of their brain when they are in a particular state of being. Therefore two people who are in the same state will most likely have brain waves that are different from one another due to the difference in the neuronal circuits themselves and the way in which the neurons fire within the individual brains. Essentially the level of specificity is due to the fact that no two people think alike.

This makes it extremely important to achieve baseline measurements of brain activity for each individual. These baseline measurements are necessary in order to determine what area of the brain is active at a particular state of being and at what frequency do the brain waves in that area need to be at in order to improve that person's state of being. Another way of thinking about it is looking at these scans in order to finding the part of the brain in which the neurons are not optimally synapsing or working together. From this it can determine which brain functions need to be targeted in order to improve a particular state of being.

All of this baseline information is used to calculate the frequency range that the individual's brain waves need to be in for optimal functioning. Once that information is plugged into the computer, the individual trains their brain to work at the frequency through the use of videogames. Sensors that measure brain waves are placed on the person's head above the area of the brain that needs to show improvement. These sensors are connected to a computer that measures the brain waves and controls the game accordingly. For example, if a person achieves the determined brain wave range a space ship will go faster however if they start to get out of the range the ship slows down. If they are no where near the correct range a black fog engulfs the ship until that brain frequency is achieved again. Without this repetitive training it is impossible to effectively alter the neural synapses that dictate the state of being a person is in.

It's easy to see how this incredible technology could help people with autism, ADD, or ADHD to focus, relax, and improve their daily functioning. Not surprisingly it can also be used to help improve the concentration and functioning of people with normal brain activity as well because this technique focuses on optimizing the way in which the neurons synapse. Essentially, this technology is used to condition and train the brain to function in a particular manner.

But this begs the question, why not use this technology to brainwash people or to train soldiers? For one this technology is highly specific to each individual; not everyone has the same brain waves and neural connectivity. Another huge problem is the fact that this technology requires a participant that is willing to do the exercises to train their brain to work in this particular way. If the person isn't willing to put in the practice, their brain won't emulate the desired wave patterns and frequencies.

The only potential way in which this technology may be used for brainwashing is if a general picture of the population's brain waves could be imaged at various states of being and placed into a generic video game. The characters in the game would only move when a particular brain wave range associated with a predetermined state of being was emulated in the player. Thus the population could essentially be brainwashed if the game was engaging enough for the participant to want to play repeatedly, the fact that the player is being brainwashed is unknown to him/her, and the sensors on their head were placed above the area in which the brain waves were being altered.

For this reason neurofeedback technology is highly regulated and restricted to mainly therapeutic purposes only. So while it is possible to play basic videogames with just your mind, the ultimate gaming experience is just out of reach due to the plasticity of the human brain and the ethical questions that lie within it.

All information was taken from:
*videos, research papers, and articles from this site were used
Posted by      Mari W. at 10:07 PM MDT
  peter pen  says:
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Posted on Sat, 27 Apr 2019 4:18 AM MDT by peter p.

Can Drugs Replace Dieting?

The Death of Dieting?

Millions of Americans try and fail to lose weight every year. Many of these failed attempts pump excessive funds toward ??fad?? diets. Sure the advertisements for these diets sound appealing: I mean it??s fast and easy right? Yet despite their glorious claims, scientific research has repeatedly shot down these diets in rapid succession. Perhaps modern neuroscience can provide the answer to losing weight with minimal effort.

A study published in the October 12th issue of the Journal of Neuroscience provides research which suggests a direct correlation between food intake, and the amount of glucagon-like peptide 1 receptors (GLP-1R) found in the core of the nucleus accumbens.

In this study, immunohistochemical and retrograde tracing techniques were utilized in rats in order to observe the presence of a multitude of GLP-1 neurons in the nucleus of the solitary tract of the nucleus accumbens. The nucleus accumbens is known to function in incentives and reward oriented behaviors, including food consumption

In order to test their hypothesis that activation of GLP-1R in the the nucleus accumbens would repress hunger, subthreshold doses of GLP-1 were injected into the core of the nucleus accumbens of the rats. It was found that up to a full day after treatment, the food intake of the rat subjects was significantly below normal levels.

Furthermore, a GLP-1 antagonist known as exendin was found to prompt episodes of binge eating when injected into the core of the nucleus accumbens in these same rats. Previously it has been observed that GLP-1 manipulation can have unpleasant side effects such as nausea, yet these side effects went unnoticed when the GLP-1 was injected into the core of the nucleus accumbens.

Past research on the brain has associated the process of food reward with structures in the rostral forebrain. GLP1 neurons are found in the hindbrain rather than the forebrain. This discrepancy suggests the involvement of both the hindbrain and the forebrain in hunger signaling.

The possibility that neuronal GLP-1 is associated with food intake seems feasible considering that it has already been accepted that intestinal GLP-1 and GLP-1R are involved in regulating food intake. That being said, it is unlikely that GLP-1 can be transported from the intestines to the nucleus accumbens due to it??s short half life, even though GLP-1 can pass through the blood-brain barrier.

The results obtained through this study did not display any significant changes in body weight over 24 hours, yet over an extended time, the results are unknown. With further research on the interconnected neuronal networks associated with satiety, it is possible that an injection or pharmaceutical could be developed to help people to reduce their food intake. Even if this never becomes a reality, learning more about satiety through research will likely help provide alternative options for overweight or obese individuals who struggle to lose weight.

For now, diet and exercise must serve as the answer for the growing epidemic of obesity in America and around the world. This study has significant implications in improving our understanding of the neuronal processes relating to satiety, and as such, it may help pave the way for future discoveries regarding the control of food intake. In any case, these experimental results stand as the first detected connection between the rostral forebrain and the hindbrain, a discovery likely to instigate follow-up studies in the future.

Source: Dosset, Amanda M. "Glucagon-Like Peptide 1 Receptors in Nucleus Accumbens Affect Food Intake." Journal of Neuroscience 31.41 (2011): 14453-4457. Web. 23 Oct. 2011. .
Posted by      Aaron R. at 9:52 PM MDT
  charlly korpa  says:
There are many drugs available in the market and they are claiming that they will help you with a rapid weight loss. But, I must say, Having drugs is not a healthy way to lose your weight fastly. There is no use of doing so and also it has many side effects.
Posted on Thu, 21 May 2020 11:06 PM MDT by charlly k.

Olfaction May Be Intimately Involved In Sexual Behavior

"They say I suffer from a lack of serotonin synapses, they happen too infrequently for me, to be functioning properly."

Neurotransmitters are a vital part of the brain, and even pop culture demonstrates a vague understanding of their importance in normal function. The scientific community embraced the importance of these chemicals decades ago, and to date, about sixty chemicals involved in neurotransmission have been identified. These range from serotonin and oxytocin to enkephalins and play integral roles in the most basic to the most complex behaviour in vertebrates and invertebrates alike. Even subtle learning mechanisms involving olfaction and sexual behavior are controlled by the same neurotransmitters, suggesting that memory is involved in sexual function. Recent evidence shows that Drosophila melanogaster may have a novel neurotransmitter controlling exactly these things, despite the fact that they seem unrelated.

Scientists at UCLA recently discovered a novel gene (which they termed prt for portabella ?? you'll understand why this is funny in a moment) that codes for a vesicular transporter and is expressed in Drosophila brain areas critical in learning and memory. This region, termed the mushroom bodies, is found only in insects and arthropods and has been compared to the cerebral cortex in mammals. Mushroom bodies are known the be active during olfactory classical conditioning, and prt has now been implicated in this learning process as well.

One important cell type in mushroom bodies are the Kenyon cells, but their neurotransmitter has remain unidentified. Various biochemical assays, including real-time PCR, velocity gradients, and density fractionation, show expression of prt's protein product, PRT, in a subset of Kenyon cells. PRT is expressed at the highest levels within larval stages, but is still present within the mature adult within axons. Interestingly, PRT is similar to both the vesicular monoamine transporter (VMAT) and the vesicular acetylcholine transport (VAChT). Dopamine and acetylcholine are found within the mushroom bodies, but neither transporter is expressed in the same patterns as PRT. In addition, although PRT is most similar to VMAT, there are subtle differences in the amino acid residues in PRT's transmembrane domains that suggest that it packages a novel substrate with some similarities to monoamines.

In order to more fully understand PRT's function in the Drosophila nervous system, mutants were created that lacked an 850 base pair portion of the prt gene. Mutant flies were then put through modified T test and exhibited impaired learning that perpetuated 30 minutes and 6 hours after training. Despite the severe loss of the prt gene, however, this learning deficit was not as drastic as expected compared to other mutants with impaired olfactory classical conditioning.

A more intriguing result of mutation in the prt gene was altered copulatory behavior. In wild-type Drosophila, males mount the female from behind, curling their abdomens to best facilitate a 20-minute copulation session. Mutants, however, failed to maintain the proper position and were even dragged around the observation chamber! The lack of proper orientation seemed to be detrimental, but only a 50% reduction in offspring was found. No genital differences were found between wild-type and mutants, so the cause of this awkward sexual behavior remains unknown. One hypothesis is that the deficit in olfactory learning impairs the male's ability to use sensory perception for proper mounting, but this has not been examined fully.

Despite controlling two seemingly unrelated behaviors, the prt gene offers a new area of intrigue within the Drosophila genome. Brooks et al. plan on continued study of the vesicular transporter in the hopes of uncovering what substrate it packages and how the mushroom bodies utilize neurotransmitters to integrate memory information and sexual behavior.

This article serves as a reminder that even some of the most understood organisms still have mysteries to uncover, as well as reminding us to continue the search for novel neurotransmitters. Even the most obscure and unrelated behaviors may be explainable by transmitters that have yet to be discovered, and hopefully Brooks et al.'s work will help nudge more of the neuroscience community towards a search for novel neurotransmitters.
Posted by      Sarah C. at 9:46 PM MDT
Tags: learning
  Sarah Cross  says:
Here's the link back to the article:

Also, fixing format on the blog was kind of a challenge with symbols for some reason...
Posted on Sun, 23 Oct 2011 9:51 PM MDT by Sarah C.
  Claire Overturf  says:
Posted on Mon, 24 Oct 2011 2:26 AM MDT by Claire O.

Technology: Virtue or Vice to Our Brains?

It is undeniable that our daily lives are inundated with technology. Our society and this world work hand in hand with technology on a close, almost dependent level. It is only in the last few decades that we have become so co oriented with technology, and it is becoming a more pressing issue than ever that we question the effects of this change. As humans, who we are is shaped by our experiences, and knowing and acknowledging this fact means we have to question both the pros and cons of such a new and close relationship with technology. When looking at this relationship it is not a question of whether or not humans are being affected by technology but how technology is affecting us.

Technology includes a multitude of different things and cannot be considered one single entity. Because it is so multidimensional it is not necessarily a good or a bad thing; a greater breakdown is necessary to determine potentially harmful technology from proven positive facets of technology. It is verified that technology as a whole has the ability to manipulate mood and arousal. It has also been proven that attention, and vision and motor skills can be enhanced while using technology. These improvements are highly dependent based on the type of technology being used and whether or not there is active or passive interaction.

Television has been around for more than sixty years but it's relevance to everyday lives and learning has never been so great. There are learning benefits to technology but three reoccurring traits have surfaced in accordance with being wired. Studies have shown that people are more likely to be violent, exhibit addictive behavior, and get distracted easier. Once again the context of the technology must be taken in to consideration. Influences of technology are starting at earlier and earlier ages these days. In children the television show Telletubbies, research showed a decrease in language proficiency in children who watched this show. However, there was a language proficiency increase seen in children who watched Dora the Explorer.

These numerous concerns and detrimental findings in research also have a flip side. New research shows indications that playing video games is associated with a number of improvements in attention, cognition, vision, and motor control. Playing video games heightens ability to pinpoint small details in chaotic scenes. Playing video games and improving these skills has shown to help people in careers such as pilots or surgeons.
Part of making technology more beneficial than detrimental is learning how to use it and how to allow it to challenge and improve our brains as opposed to letting it become a route to mindlessness. We are seeing that the attractive features of video games such as emotional context, arousing experiences, and richly structured scenarios are what boost our intellectual brain and educational technology tends to exploit the repetitive nature of practice makes perfect. Making moves to shift educational technology toward the more interactive nature of technology could only improve our relationship with technology. It is difficult to study the ways that technology affects the human brain but considering the growing reliability and interaction humans have with it, research in this field is both necessary and critical to society.

Full article can be found at
Posted by      Bethany B. at 9:41 PM MDT
displaying most recent comments (8 ommitted) | Comments (11)
  Litta John  says:
Posted on Tue, 26 May 2020 6:28 AM MDT by Litta J.
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  robert frcrocke  says:
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Will this Blog Affect How you Read the Rest?

It's intuitive that memory and perception are linked, but the underlying neural mechanisms for this interaction are still unclear. The article "Biasing Perception by Spatial Long-Term Memory" (Summerfield et al.) from the Oct. 19th issue of The Journal of Neuroscience sheds some light on this problem. Their experiment links previous visual perception and subsequent long-term memory generation to increases in brain activity, improved behavioral performance and enhanced perceptual functioning in a recall type task.

This linkage was uncovered by putting subjects through visual identification tasks. The tasks involved finding a gold key, which was inserted into a complex picture after a random short period of time. The subjects were put through 160 trials in one day. These trials were setup in a precise manner that enabled the experimenters to strictly focus on the task and relevant results. EEG recordings, reaction time, accuracy, and optic focus were measured. The next day the subjects were put through the task again. With a number of the trials replicating the previous picture and key location exactly.

The experimenters analyzed the results prior to the experiment and eliminated the outliers and bad trials. The results demonstrate "anticipatory spatial biases were triggered by long-term memory" (5). Long-term memory affects the early stages of visual perceptual processing. The experimenters recorded increases in brain wave activity that mimicked the activity seen in trials where the subjects correctly identified the key on the first day. So when the same picture and key placement were used on the second day the brain wave activity of the first day was replicated before the stimulus was presented. This anticipatory affect is due to the long-term memory prepping the visual system for the expected target.

This study is helpful in generating a greater understanding of how powerful our long-term memory is. It inadvertently points to the possibility of problems that may arise when people find themselves in similar scenarios. The long-term memory bias was beneficial in the case of the study (faster reaction times), but these preconceived ideas may send some down the wrong path in a different scenario. The long-term memory's influence on perception may promote greater speed and fluidity in simple tasks, but what other assumptions and conclusions will it lead people to jump to. Is long-term memory bias causing people to make quick irrational decisions based on what worked last time? What other aspects of perception and action are being affected by long-term memory bias? To what extent do scenarios have to be similar to allow for this anticipation effect? Is this evolutionary adaption losing utility in a world that requires more imagination, understanding, critical thinking, and thoughtful interaction due to technological innovation and globalization?

All these questions and many more are on the cusp of discovery. This article uncovers a key building block to deciphering this neural pathway. Their use of EEG demonstrates the utility of this technique to answer questions about spatial and long-term memory. Applying this technique to novel scenarios will increase our knowledge of memory's role in biasing perception.

The Journal of Neuroscience October, 19th 2011
Posted by      Charlie S. at 9:31 PM MDT
Tags: eeg, learning, memory
  Heather Skye  says:
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  zaiya mariya  says:
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Posted on Wed, 20 May 2020 3:05 AM MDT by zaiya m.

Reimagining Alzheimer's Disease�??An Age-Based Hypothesis

Seth Graban

Everyone realizes that as grandma or grandpa ages they become more forgetful, but at what point is this forgetfulness a result of age or a result of something else such as Alzheimer�??s. This mentally deteriorating disease arises more often by chance than through familial and this correlates with new data available to biomedical researchers. This is why a full review of the origins of Alzheimer�??s is being performed. The review of Alzheimer�??s disease resulted with three primary factors that work in correlation to result in the disease. An initial injury results over time leading to a chronic neuroinflammitory response, and this response can eventually lead to a discontinuous cellular change in state involving most brain cells.
The initiating injury doesn�??t necessarily need to be a specific event such as a fall or trauma to the head; it may be built up stress with age or an infection/illness. Though the primary initiating injury is believed to be a vascular even such as head trauma or a micro stroke, all injuries cause a protective response. Age plays a key role in regards to a protective response because with age comes failure of homeostic mechanisms. This means the protective response to the injury continues, even if the injury itself abates. A very important note is if research can identify the most common sources of injury, then there may be a way to intervene the onsets of Alzheimer�??s.
Inflammatory response resulting from an initiating injury follows tissue damage, but there is a distinct relationship between Alzheimer�??s and chronic inflammation. Because age results in failure of homeostic mechanisms, chronic immune response persisting over a long period of time creates the unique chemistry and cellular physiology, a marinade if you will, that results in the symptoms of dementia in Alzheimer�??s. Since inflammation is a key cause of Alzheimer�??s, long term high-dose anti-inflammatory drugs may lower the lifetime risk of Alzheimer�??s by 30-60 percent but further research needs to be done to study possible side affects.
Both the initiating injury and chronic inflammation lead to the onset of Alzheimer symptoms of dementia, but at what point is it Alzheimer�??s or age? The answer to this question says there needs to be a functional discontinuity between early and late stages of Alzheimer�??s, a point in which a cell cannot change back to the previous functions. Naturally with age early symptoms of Alzheimer�??s may arise by chance but it is the turning point of the cell that causes grandma to not remember your name. When the cell changes, a �??new normal�?? is established. This �??new normal�?? includes processes for over-stimulation of autophagosomes that lead to cell death. This is why neurons at risk for death in Alzheimer�??s patients show defects in autophagic functions.
Relating these three factors of Alzheimer�??s, it is the nature of the response and not the nature of the injury, which causes the chain reaction leading to the disease. As a result of these findings, researchers have been reviewing other neurological diseases and reexamining them to establish differences in current research with prior research. Many correlate with Alzheimer�??s in the matter of the initiating injury and the inflammation, but the final mutation path the cell takes determines the type of neurological disease established.

Posted by      Seth G. at 9:22 PM MDT
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Posted on Thu, 21 May 2020 3:50 AM MDT by zaiya m.

Seasonal Depression: Connecting Immunology and Neuroscience

In the United States, depression has quickly become one of the most well known and most common mood disorders. The notoriety of this disease has certainly come about due its prevalence in society and how it affects the afflicted. Depression can have devastating effects on a person, so it naturally has become a hot area in research. Seasonal affective disorder is a subset of major depression that afflicts people in different seasons due to a change in the amount of light in a day. A large number of residents in Alaska, for example, suffer from this disorder due to the few hours of light they receive during certain times of the years. Perhaps this seasonal depression risk, along with the burden of listening to a certain political figure, is a reason Alaskan residents receive an annual stipend for living where they do. In order to understand this form of depression further, a group at the Medical University of Vienna studied the relationship between immune system proteins and seasonal depression.

Depression has been linked to altered circadian rhythms, and, subsequently, altered levels of immune system elements like cytokines, specifically interleukin 6 (IL-6). In the immune system, cytokines promote inflammation in areas where they are produced. To observe the affects of light deprivation the researchers deprived mice of light and determined their depression and cytokine levels. The light deprived mice showed depression-like behaviors when subjected to depression distinguishing tests. Furthermore, these mice with traits relating to depression showed elevated levels of IL-6 in circulation and in hippocampal cells. To further understand this increase in the pro-inflammatory cytokine IL-6, the researchers observed the effect of NF-kB, which is a transcription factor for IL-6. Discovered in these mice were elevated levels of DNA binding by NF-kB which supports the evidence that there are higher levels of IL-6. In order to further implicate the role of IL-6 in seasonal depression, IL-6 knock out mice were exposed to the same light deprivation as the control mice. These IL-6 knock out mice showed lower levels of depression-like behavior, which tells us more firmly that IL-6 cytokines play some sort of role in seasonal depression.

These studies could potentially provided huge implications in the world of seasonal affective disorders. Since light deprivation was shown to activate NF-kB and therefore production of IL-6, one may think we could simply inhibit this pathway. The problem with this would be the severe negative implications on the immune system. These cytokines that NF-kB activate are crucial for fighting infection and maintaining a healthy individual. Without them, an organism would quickly be riddled with infections that they could not control. Although the study does not provide an immediate treatment for seasonal depression, we are provided beneficial knowledge that takes us a step closer to finding a better form of treatment. This link between immunology and neuroscience also provides more incentive to study this relationship in other neurological diseases and provide more treatments for diseases that affect so many people.

Source: Constant Darkness Induces IL-6-Dependent Depression-Like Behavior through the NF-κB Signaling Pathway
Posted by      Kyle D. at 9:21 PM MDT
Tags: depression
  charlly korpa  says:
If we are having the same mood order due to depression at a particular time of every year is called seasonal depression. It is also called as Seasonal affective disorder (SAD). Cellular Signal Booster Talk therapy and medication is the best treatment for this kind of ill state.
Posted on Wed, 20 May 2020 10:34 PM MDT by charlly k.
  Jack William  says:
Depression is a part of life and we have to face it in different ways and that's not easy. The
assignment help perth share some of the books which you can read at the time of depression and cool your mind at that time.
Posted on Thu, 28 May 2020 3:08 AM MDT by Jack W.

Predator or prey, your amygdala doesn't care

As a child, did you ever come across an animal you had never seen before, say a small, harmless mouse, and felt highly alert, maybe your heart started racing or you felt nervous, despite knowing nothing about the animal? Or perhaps you remember being strongly drawn to an animal like a puppy at a young age, more so than an object like a toy? A recent study published in 2011 has found that there may just be a neurological explanation for our heightened emotional responses to animals.

This experiment recorded neuronal activity from three regions (the amygdala, hippocampus and entorhinal cortex) of the medial temporal lobe in 41 neurosurgical patients as they viewed a series of four different stimuli, either landmarks, people, objects or animals. The results researchers observed were quite interesting. Of all three medial temporal lobe regions, the only region to show significant selectivity to any stimulus was the amygdala. Knowing this, what stimulus would we think the amygdala might be most highly specific for? Well, we know that the amygdala plays a primary role in arousal, emotional responses and fear, so it shouldn�??t be surprising that results concluded there to be a highly significant selectivity (P< 10-15) for animal images in the neurons of the amygdala. These neuroscientists then tested for differences in neuronal responses between the left and right amygdala by repeating the above experiment separately on each section of the amygdala, concluding that the observed category-specific response arose solely from the right amygdala.

Now that we know the amygdala is selective to animal images, we might wonder, do some animals generate a more significant response than others? For example, does an image of a lion or other dangerous, life-threatening animal evoke a higher response than an image of a small, cute animal like a rabbit or a kitten? Surprisingly, no! Researchers found no relationship between the amygdala responses and the characteristics of the animal. So if some stimuli are more threatening than others, why don�??t they evoke a higher response? An evolutionary explanation for this is the concept of predator vs. prey, where each stimulus has its own significance as either posing as a threat, or posing as a potential meal. Because each of these is so crucial to survival, our brains have evolved to hold specific processing for this category of stimuli.

With this knowledge, the next question is, is there a category-specific response in other animals as well? And if so, does it differ among animals based on their hierarchal position as a predator or prey?

Source: Nature Neuroscience: A category-specific response to animals in the right human amygdala
Posted by      Hannah M. at 8:14 PM MDT
Tags: amygdala

Are Placebos the New Painkiller in Sports?

The use of painkillers in sports is not a new phenomenon. Nearly every NFL player you see on Sunday likely has something in their system; letting them momentarily forget their pain and subject their bodies to blow after devastating blow. Whether it??s a couple of Advil or a cortisone shot to an ailing right shoulder, players constantly use substances to divert the pain.

The NFL and all other major sports corporations have policies that attempt to keep this type of drug use under control. It is illegal to take shots of morphine before a game, for example.

Players today are no longer limited to direct injections to experience the positives of painkiller, however. A study posted in The Journal of Neuroscience has provided evidence that placebos can meditate the effects of opioids. This means that, using opioid conditioning, an athlete could experience the physical response of an opioid without actually taking the drug on the day of competition.

In the study athletes were given administrations of morphine during what they called the precompetition training phase. When game day arrived they were given a placebo instead of the typical morphine administration they had become used to. The researchers found that the placebo induced an opioid-mediated increase of pain endurance and physical performance.

In other words, the athletes were essentially on morphine without actually taking any morphine.

The study involved four different groups of healthy males. Two groups were trained with morphine injections while the other two groups were trained without morphine. On the day of competition, one of the conditioned groups was given a placebo morphine injection and one of the unconditioned groups was given a morphine injection.

The conditioned group who was given a placebo on the day of competition outperformed the other three groups in the pain tolerance tests by a statistically significant amount of time.

This finding, along with other findings from placebo studies, suggests that combinations of placebos and verbal suggestions of drug administration can activate the same neurotransmitters in the brain that are activated by the drug.

This is clear evidence of how the placebo effect works schematically inside our heads. Our brain encodes needle injections and phrases such as ??time for your morphine shot?? as stimuli to activate chemical release.

The question now becomes is this type of conditioning legal? The players are not actually taking banned substances on days of competition, and as the article points out, morphine is a banned substance only during competition.

Is the athlete actually cheating by conditioning their brain? This is not as clear as with the case of steroids. It seams much easier to draw a conclusion that an athlete is gaining a physical advantage by putting on more muscle that would not otherwise be possible without the use of a steroid. In many ways the placebo effect gives athletes an otherwise unobtainable pain tolerance.

It will be interesting to see if this type of conditioning will be used regularly in professional sports. It is likely that and induced opiate response could have noticeable effects in endurance sports such as cycling and track and field events.
Posted by      Sean F. at 8:02 PM MDT
  Christina Uhlir  says:
Did the article get into the ethics of deception at all?
Posted on Mon, 24 Oct 2011 6:37 PM MDT by Christina U.
  Hering ering  says:
Neuro science responsive articles I have got for best conditioning on brain. The academic writing services reviews really help us to gather interesting articles on steroids and athletes.
Posted on Wed, 20 Mar 2019 1:34 AM MDT by Hering e.

Practice Makes Perfect

We have all heard it, whether growing up playing sports, music, or some other activities requiring motor function; "practice makes perfect". How you practice is how you will perform. And if you learn something the wrong way and are never corrected, it is extremely hard to change. But if you continually practice and are corrected, it is much easier to catch on and become closer to perfection. But does the way in which we practice really have that much of an influence on how we retain what we have learned and our overall performance?

A study recently published in The Journal of Neurobiology provides evidence showing that the structure of the initial phase of learning has an enormous influence on the ease of motor relearning. While other studies have shown that training with random practice leads to better retention that blocked practice, the researches in this experiment desired to learn if practice structure also affected motor adaptation.
In their study, the researchers observed fifty-two healthy volunteers walk on a custom built treadmill that had a split-belt walking adaptation in order to determine if changing the training structure affected retention.

The researchers performed two experiments. In the first, subjects were exposed to the split belt, and then assigned randomly to one of four groups. The groups varied in the split-belt training paradigms in order to asses the effect of switching walking patterns with repeated bouts of adaptation and to investigate whether the breaks between split-belt periods were important for re-adaptation. They then returned twenty-four hours later to measure the next day re-adaptation.

In the second experiment, the researchers tested to see if learning the opposite split-belt pattern caused a delay on recall, relearning, or performance when they were brought back for the next day re-adaptation.

In the first experiment, it was found that walking adaption was remembered on the second day. Also, it was discovered that the training schedule did, indeed, have an affect on the relearning on the second day. The results in experiment two did not differ from that of the first.

While most of us do not care to learn how to walk on a split belt treadmill, nor it's affects on our learning, we can at least learn something from this study. The way in which we practice or learn a specific motor task does have an affect on how we continue to perform in the long term. When we are repeatedly trained a certain way, it is easier for us to retain that experience from day to day. But if we are suddenly taught another way, it becomes harder for us to retain the first. Yet if we are repeatedly taught the two ways in alternating intervals, relearning comes easier for both tasks.

So, next time you find yourself practicing, think hard about how you are performing and if you are trying to teach someone how to do something, be patient with them and take many breaks for the best overall performance.,
Posted by      Ashlyn C. at 6:40 PM MDT
displaying most recent comments (2 ommitted) | Comments (5)
  Christina Uhlir  says:
Sounds mildly uncomfortable.
Posted on Tue, 25 Oct 2011 5:43 PM MDT by Christina U.
  Ashlyn Carney  says:
Yes, I would think so and the subjects wore a safety harness.
Posted on Wed, 26 Oct 2011 8:56 PM MDT by Ashlyn C.
  Christina Uhlir  says:
I, personally, would feel quite ridiculous doing that sort of activity.
Posted on Thu, 27 Oct 2011 7:54 AM MDT by Christina U.

Internet Media Educates us as Traditional Media Never Has

At this point in time there is a staggeringly vast amount of knowledge available to people through the internet. There is now so much knowledge available that this particular time period has earned the moniker ??the information age?? and is considered distinct and special due the widespread availability of this knowledge. For informal and underground fields of study or interest this is a great boon. For the first time in history these fields of study are given a set up where the few and far between collaborators can easily communicate, cooperate and disseminate their results to the interested amateur. In technical fields with a high barrier to understanding such as biology and neuroscience, the ease of passing on information through the internet is cutting out middleman news distributors and producing sources of intelligible information produced by people who are experts in their fields.

Traditionally much of the public has gotten its science information from newspapers, magazines and television news programs. These sources, run by journalist who study and focus on distributing information to the public are excellent at catching the public eye and producing results that the public finds interesting. However, journalists often lack significant scientific backgrounds or training, and therefore are not always qualified to interpret the science they are publicizing. The result has been that historically the public has often been fed simplifications of scientific matters, or occasionally misinformed entirely.

Now that scientists have gained access to the internet for distributing information, the public has new and more expert venues for learning about whatever science interests them. Blogs written by scientists are available for most scientific topics, while social media sites often have sub sections dedicated to the discussion of news within various sciences. Surprisingly, despite the amateur nature of many of the content contributors, the content is often just as readable as what can be found in traditional sources such as newspapers and magazines. It is however more expert, increasing the quality of the information available to the public.

Another aspect that internet media brings to the table which has never previously been available is an element of interactivity between content creators and content consumers. The brilliance of social media lies in the fact that users can request clarification or increased depth directly from the producers of content. There are even sites which focus on increasing public knowledge by creating a forum between laymen and scientists on scientific topics. The website has a subsection for this called askscience (, which has over the past month discussed scientific questions varying from the whether IQ differences can be estimated through brain imaging to how big stars can get.

Traditional media outlets will continue to be an important purveyor of scientific conclusions by summarizing large issues in science and reaching the general public at large. However any laymen interested in scientific knowledge, internet media is providing opportunities never before seen from the traditional side of science journalism. With its potential for in depth expert analysis and discussion between scientists and the curious, the internet has greatly improved the quality and availability of scientific knowledge.
Posted by      Michael A. at 5:33 PM MDT
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  Nathan Jones  says:
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Posted on Mon, 9 Mar 2020 9:31 PM MDT by Nathan J.
  Emily Nelson  says:
Thank you for sharing your insights! Yes, the internet has brought a lot of benefits to our way of living, including the acquisition of information. It has also opened doors for content to be shared in a way people can have access to it. Inspirational videos, podcasts and books can also be found online. TedX speaker Sydney
Posted on Tue, 10 Mar 2020 12:52 AM MDT by Emily N.
  Chloe Summers  says:
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Posted on Tue, 10 Mar 2020 9:17 PM MDT by Chloe S.

Glutamate Increase Elicits a Genital Response

Ever since I was a little kid, whether I was in sex ed., at home or at a friends house, there was some voice telling me that men are stimulated visually. There is no doubt in my mind this is true. Just walk down the magazine isle at a grocery store, or flip on the TV for more than ten minutes. Most women are displayed wearing next to nothing, whether in a bikini or revealing clothing. All of this is done in an attempt to sell the product. Its no wonder a lot of marketing companies are under the impression that sex sells, because it really does. But why? It cant be that men are simply sex hungry pigs, who only see women as objects of their pleasure. Maybe that is true for some of us, but there has to be something more going on. What even controls this sex drive in men and how is it increased or decreased by our outside environment?

Note: For the purpose of this article we are going to be talking about the sexual experience from a heterosexual viewpoint. It can be applied across any type of sexual relationship, but the premise for this research is based on heterosexual coupling.

Todays research on the male sex drive points to the medial preoptic area (MPOA), which is found in the hypothalamus. The MPOA is seen as the critical regulatory site for the control of male sex behavior. The MPOA does play a role the female sex behavior, but is reported to be larger in males than in females. In a paper titled Preoptic Glutamate Facilitates Male Sexual Behavior, Juan Dominguez and his colleagues at Florida State University take a stab at the neurological basis for the male sex drive. What they did was measure glutamate levels in the MPOA, before, during and after copulation in male rats. Their results showed that when the female was presented (the rats received a visual stimulus), the extracellular glutamate levels rose 140% of the baseline level. During the actual time of sex the glutamate levels rose 170% of the baseline level, and during the time of ejaculation, the glutamate levels rose an astonishing 300% of the baseline level. Immediately after ejaculation, glutamate levels decreased rapidly. Dominguez and his researches tied the fall in glutamate to the length that the individual remained at inactive or at rest after the time of ejaculation.

So why does any of this matter? Well when trying to tackle the male sex drive, this information is important. What women wear and how they present themselves has an effect on how men think and how their body reacts. A scantily clad woman can elicit an extracellular glutamate increase and an overall increased sex drive. This can have huge implications on the behavior of that individual. Now the sex drive is not only increased by the feelings the individual may experience in response to the stimulus, but has actual physical implications. Dominguez concludes his research by saying that glutamate in the MPOA can elicit genital reflexes in anesthetized rats.

I believe that there is some level of control that men have on their sexual behaviors, but mens bodys neurologically respond automatically, whether they like it or not. So ladies, the next time you are getting ready to go out, putting on perfume and deciding what to wear, realize that what you put on is part of how you want to be perceived. The actions you make, whether you flirt and tease or spend your night reserved and in conversation, alter the sex drive of men. In other words, men are going to neurologically respond according to the stimulus put in front of them. If you want to increase his sex drive, do not wear very much and touch him a lot, as he will most likely be hoping to hit that 300% of baseline. But if not, you can help control his sex drive by dressing and acting accordingly. Just as was stated to me my whole life, men are visual beings.

This is in no way a justification for the cases in which men have disrespected and abused women because what men experience and how they respond to it are two very different things. But there is a definite benefit in understanding the neuroscience behind what spurs on the male sex drive and how that can be maintained and regulated by outside stimuli.

Dominguez, Juan M., Mario Gil and Elaine M. Hull, Preoptic Glutamate Facilitates Male Sexual Behavior, Journal of Neuroscience (2006): 1699-1703;
Posted by      anthony b. at 5:27 PM MDT
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How You Mother Has Eyes on the Back of Her Head

By all accounts Katie Joe McDonough was the least likely woman to rear progeny. She was independent, stubborn, and adventurous; nothing would hold her back. Her twenties were a thrill ?? packed with adventures to India and Nepal, learning French and moving overseas to work for a French oil company, the pursuit and completion of a PhD in Geophysics, and countless hiking, trekking, and boating trips. Katie Joe would not ??settle down.?? My Dad can attest to this ?? he barely got her through the chapel door. Pregnancy didn??t change anything ?? my mom was in denial for the first four months she was pregnant with me. But the day that I was brought naked and screaming into this world my Dad describes an incredible change that came over my mom. She softened. The minute her senses registered my existence all hesitance was gone. She became uncharacteristically tender. ??She got boring!?? my brothers and I describe with delight. She became a mother.
Evolution favors this kind of maternal transformation in new mothers ?? especially among mammalian females. As soon as the babies arrive, Mom??s senses must kick into overdrive. She now has much more to worry about than her own survival. She is now responsible for feeding, protecting, and teaching her offspring, and that takes a massive amount of increased brain function. Adi Mizrahi and his colleagues from the University of Jerusalem have begun to investigate some of these changes in the brains of mouse mothers. Through research on sensory integration between auditory and olfactory neurons in the brain, Mizrahi et al has uncovered evidence that suggests that specific brain plasticity is triggered in mouse females in response to their offspring. Sound familiar? I don??t know about yours, but my Mom can always tell when my hand is reaching into the cookie jar ?? even without turning around.
So what is responsible for this increased vigilance in new mothers? Mizrahi??s experiments demonstrate that in mouse mothers, specific sensory neurons exhibit increased plasticity in response to stimuli from mouse pups. This plasticity causes increased integration between sensory systems leading to hyper-vigilance in the mother. In the Mizrahi experiment, over 400 auditory neurons in new mouse mothers were tested for excitation in response to a variety of frequencies in the presence of (a) fresh air and (b) in the presence of their pups?? odor. Mizrahi??s findings demonstrate an overwhelming increase in the auditory neurons of new mothers in the presence of pup odor. In addition, the auditory neurons tested did not show the same increased responsiveness to neutral sounds. Instead increased activity in the neurons was triggered by the specific frequencies of mouse pup distress calls. This integrated response to pup calls and odors was not found in virgin female mice. But interestingly, the virgins did begin to show increased integration after prolonged exposure to mouse pups. This suggests that sensory integration plasticity in mice is not triggered by the actual act of birthing offspring, but may instead be linked to exposure to mouse pups. Maybe a similar phenomenon is responsible for the uncontrollable ??Awww!?? that pours from my mouth every time I see a picture of Jared Polis?? s new baby.
Posted by      Stephen B. at 4:47 PM MDT
  Stephen Blaskowski  says:
Source: Lior Cohen, Gideon Rothschild, Adi Mizrahi;
Posted on Sun, 23 Oct 2011 4:50 PM MDT by Stephen B.
  Christina Uhlir  says:

I must admit to a certain degree of confusion, was there no mention of oxytocin in the article you read?
Posted on Sun, 23 Oct 2011 5:21 PM MDT by Christina U.

The Mystery of Autism

The cause of autism has been an ongoing debate for years, but has recently become a hot topic due to technological advances in the field of neuroscience. Previous to these advancements, autism was investigated and treated based on purely behavioral criteria, making the cause difficult to identify.

Before diving into the complex neuroanatomical abnormalities that accompany this disorder, it is important to identify the deficits/symptoms that signify this diagnosis. Clinically, autism presents with what is called a triad of deficits. This includes impaired social interaction, impaired communication, and restricted interests and repetitive behavior. Communicational impairment can range from under development of speech to no speech at all. Children with autism often have difficulties coordinating attention between subjects of mutual interest, often causing problems in social environments.

Studies being conducted by Matthew Belmonte and his research team have found abnormalities in neuronal connectivity in patients with autism. According to their study, autistic brains experience high local connectivity in tandem with low long-range connectivity (Belmonte et al., 2004).

Using functional magnetic resonance imaging (fMRI) and EEGs, they were able to visualize the abnormally large activation from sensory inputs but a reduction in the selectivity of this activation. The long-range connectivity showed reduced activation. According to these studies, the brain region experiencing this increased activation is the parietal cortex, while the prefrontal and medial temporal cortices experience low activation (Belmonte et al., 2004).

Interestingly enough, non-autistic brothers of people with autism show the same prefrontal and medial temporal inactivity but do not show the increased activation in the parietal cortex. This suggests a familial pattern of brain organization and a possible phenotype that increases ones risk for autism.

Another anatomical structure that is said to play a central role in autism is the cerebellum. Recent studies show that in autistic individuals, cerebellar activity is abnormally low during tasks of selective attention and abnormally high during simple motor tasks. A reduced size of cerebellar sub regions also correlates with a reduced number of Purknje cells. This would result in the release of deep cerebellar nuclei from inhibition, which would in turn lead to strong physical connectivity and weak computational (Belmonte et al., 2004).

Furthermore, studies of the cerebral cortex in autistic individuals indicate abnormalities of synaptic and columnar structures and of neuronal migration, and even increased total brain volume (Casanova et al., 2002). Strangely, autistic children showed abnormally large brain volume while adults with autism did not. This is said to be the result of early hyperplasia followed by a plateau during which normal growth catches up. The areas of the brain most affected by these abnormalities are those in which project broadly to other regions that play a key role in attention, social behavior, and language. This coincides with the idea of local hyperactivity and long-range hypoactivity.

While the physical abnormalities are being uncovered piece by piece, the cause of these abnormalities is still a debate amongst neuroscientists. Belmonte's research and findings are a key stepping stone to a possible cause and treatment of this mysterious disorder.

Belmonte, K. Matthew et al., Autism and Abnormal Development of Brain Connectivity. The Journal of Neuroscience, October 20, 2004.
Posted by      Madelyn K. at 4:28 PM MDT
  Christina Uhlir  says:

Thank you for not mentioning MMR vaccinations as a possible cause, though I doubt the article would even give that hypothesis the time of day.
Posted on Sun, 23 Oct 2011 5:27 PM MDT by Christina U.
  Gino Ciarroni  says:
I wonder how you can use the article to inquire about pharmacological remedies/aids for autism. I have always been interested in the linkage or similarities of Attention disorders vs Autism, relating to executive function or attention. For example, findings suggest that variations in a gene on 16p13 may contribute to common deficits found in both ADHD and autism. Another experiment Method:?? Three rigorously diagnosed groups of children aged between 6 and 12 years (54 ADHD, 41 HFA, and 41 normal controls) were tested on a wide range of tasks related to five major domains of executive functioning (EF): inhibition, visual working memory, planning, cognitive flexibility, and verbal fluency. In addition, the role of comorbid oppositional defiant disorder (ODD) and comorbid conduct disorder (CD) in ADHD was investigated by directly comparing 20 children with ADHD and 34 children with comorbid ADHD + ODD/CD.

Results:?? ADHD was associated with EF deficits in inhibiting a prepotent response and verbal fluency. Children with HFA demonstrated deficits in all EF domains, except interference control and working memory. The HFA group showed more difficulties than the ADHD group with planning and cognitive flexibility. The comorbid ADHD + ODD/CD group did not show a distinctive pattern of performance on the EF tests compared to the ADHD group.

Conclusion:?? The present study indicates that children with HFA exhibit more generalised and profound problems with EF tasks compared to children with ADHD.

So while autism seems to be a more server deficit on executive function, can use ADHD or other EF disorders as a model to study Autism? Can use it as model for pharmacological intervention to decrease severity of symptoms?
Posted on Fri, 28 Oct 2011 12:18 PM MDT by Gino C.
  Gino Ciarroni  says:
Sorry bout the formatting errors!!! Cant delete post to retype.
Posted on Fri, 28 Oct 2011 12:19 PM MDT by Gino C.

Flies Like to Get Drunk As Well?

Well, it is unclear whether they get "drunk" or not but they do display hyperactivity after being exposed to intoxicating vapors of ethanol which is similar to that of what humans do after drinking too much. A recent study done by Karla R. Kaun et al shows that flies are attracted to ethanol just as much as humans are. Although humans have various reasons for ingesting alcohol, flies on the other hand, are attracted the rewarding effects that ethanol has on the brain. This attraction towards ethanol and the rewarding effects are so great; one could say that they are addiction to ethanol.
In the study done by Karla R. Kaun et al, they wanted to test whether or not flies displayed addition like behavior such as that in humans. They conditioned flies to be attracted ethanol by various means and tested them for addition like behavior by administering 100 V and 120 V shocks. They found that even after administering shocks to the flies, they were drawn to ethanol. Another test was done with the same voltages except ethanol was replaced with sucrose. This time, the flies only tolerated the 100 V shock and not the 120 V shock. This higher tolerance towards ethanol than sucrose could mean that they associate ethanol as giving them a more rewarding feeling than sucrose and that ethanol is worth the pain.
The flies were, as one could say, addicted to ethanol but why was this? Well, as we know, dopamine plays a role in the reward system and "ethanol amplifies the dopaminergic responses to natural reward and reward-related environmental cues" which causes this attraction and who can blame them, we all like to feel good (Karla R. Kaun et. al, pg. 3). Not only does dopamine play a role in the reward system, but so does memory of that good feeling. Karla R. Kaun et. al also found that the mushroom body and scabrous gene were required for the ethanol reward memory. By blocking various synaptic transmissions in the mushroom body, they found that the formation of ethanol reward memory "may be mediated by dopaminergic innervations of the αβ neurons (Karla R. Kaun et al, pg 5)." Karla R. Kaun et al also found that within the mushroom body, there was the scabrous gene that was required for the ethanol reward memory. It plays a role in this reward memory in that scabrous sends signals to Notch in which Notch mediates the reward memory. And so with the brain releasing chemicals that make you feel good and memories of that good feeling, who wouldn't be addicted to something that made you feel this way?
So why does studying flies and their addiction towards ethanol matter? Well, by studying flies and what influences them in their addictions, it could help researchers better understand human addiction and possibly allow researchers to find ways to help people with these addiction such as finding genes or circuits that makes a person more susceptible to being more addictive to various substances. By being able to identify these factors that influence a person's addiction, there will be better ways of treating a patient who has a drug abuse/addiction problem and better ways of treating the side effects of going off the drug such as withdrawal.

Posted by      Kou X. at 3:14 PM MDT
  Christina Uhlir  says:

What is the mushroom body, scabrous gene, and Notch?
Posted on Sun, 23 Oct 2011 5:48 PM MDT by Christina U.

One Prick and you are Out

Isn't it crazy with one prick of anesthetics you can be out and then awaken hours later and have no recollection of what just happened? Sleep is like this too except, you have to close your eyes for a little then all sudden "poof", you awake to a morning sun. Sleep and anesthesia seem to be one in the same, but in reality they are not. Researchers in Canada measured the long field potentiation and coherence of cortical neurons in anesthetize and sleeping cats to investigate the differences.

Slow wave sleep (SWS) or what we call sleep is characterized by sleep slow oscillations, a characteristic of anesthesia. These oscillations form by cortical cells alternating between depolarizing and hyperpolarizing states. Depending on these oscillations neurons can either be active, a state of high synaptic activity or a silent state, low synaptic activity. Both aestheticize cats and sleeping cats were found in silent states but the amount of time aestheticizes cats were in the silent state differed.

Cats in SWS were found to have irregular slow waves or slow oscillations within each of the recorded cortical regions. When the anesthesia Ketamine- xylazine was injected into the cats, these regions showed consistent slow oscillations. These findings concluded that during SWS not all the brain regions are in silent states or inactive, so in sense, the brain still can processes information from the outside world. Opposite of that, aestheticize cats cannot process information because most the brain regions are in an inactive phase. So when a person receives anesthetics for surgery, they are not able to process that surgeons are cutting open their bodies, compared to a person who is able to wake up in the middle of the night because he or she processed that there might be a fire outside.

With the use of three different frequencies, regions of the brain could were investigated whether there are synchronous or non synchronous activities in the brain during the SWS and anesthesia. Aestheticized cats were found to have synchronous frequencies in contrast to nonsynchronous activities in SWS cats. These findings explain why a person can recall some of their dreams when they wake up compared to a person waking up from receiving an anesthetic. Because slow waves start to decrease as a person is about to wake up, there is a point in time where the active state is a little longer than a second, allowing a person to somewhat recall their dreams. While when someone is under anesthesia, the time in silent state is double compared to SWS. Synchronous brain activity allows for not time for regions of the brain to become consciousness during the transition from silent to an active state.

With these finding it hoped that further investigation of consciousness and unconsciousness could be understood. With many patients under comas for many days, months, and years, wouldn't it be a miracle if there was a way to wake them up?

Chauvette, Sylvain, Crochet, Sylvain, Tinofeev, Igor, Volgushev, Maxim. "Properties of Slow Oscillation during Slow- Wave Sleep and Anesthesia in Cats." The Journal of Neuroscience. 31 (2011)
Posted by      Erika L. at 2:33 PM MDT
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  Christina Uhlir  says:
Sometimes I think Wikipedia is a credible source. 12 hours seems like a tad of an underestimate for my fat cat. :)
Posted on Mon, 24 Oct 2011 5:27 PM MDT by Christina U.
  milan joy  says:
Before any critical surgery, it is a common procedure that doctors Internet of Things give anesthesia to the patients. You are become unconscious for certain hours after this anesthesia given. It was so nice to see this article that share the details regarding it.
Posted on Mon, 9 Dec 2019 10:51 AM MST by milan j.
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Jalapenos...a treatment for arthritis?

We've all bitten into a jalapeno and experienced the slow burning pain that is associated with it. And whether you love it or hate it you've probably wondered why some people have a higher tolerance for spicy foods than others. The answer to that is two-fold.

To understand why we must first understand the mechanism through which capsaicin (the oily substance found in peppers which gives them their signature 'kick') works. Capsaicin targets a subgroup of sensory neurons called nociceptors. Prior research has shown that capsaicin excites these neurons by increasing the permeability of the plasma membrane to cations (K+, Na+ and Ca++ in particular) although it was unknown whether this was through direct disruption of the plasma membrane (capsaicin is hydrophobic and could thus perturb the phospholipids of the membrane)or though a ligand-system in which the molecule binds to specific receptors on the surface of the cell. The latter possibility was ruled more likely as capsaicin derivatives operate in dose-dependent manners highly characteristic of receptor activation via ligand binding. This was further supported through the use of resiniferatoxin, an extremely potent capsaicin analog derived from the plant genus Eurphorbia. This neurotoxin's extreme potency, eliciting responses at nanomolar concentrations, allowed scientists to assume that it bound with great affinity to the proposed capsaicin receptor. Using this, the molecule was radio labeled and researchers were able to visualize its binding to cell-surface receptors.

This provides the first the leg of the answer. The density of these receptors on an individual's nociceptors can influence the affect spicy food has. More receptors, more binding, greater response evoked.
An interesting side note...why do spicy foods produce a burning sensation? The specific receptors that capsaicin binds to are heat-gated receptors. These are analogous to our very well known voltage-gated channels but open is response to changes in ambient temperature and apparently capsaicin binding. This produces pain and the burning sensation that I for one love.

The second leg to our answer comes with a remarkably interesting point of immense pharmacological importance. Exposure to capsaicin initially excites a neuron leading to the pain response. However prolonged exposure (in this paper just a few hours) can cause cell death. Examination of dead cells revealed no evidence of DNA fragmentation meaning that no apoptotic events occurred. The actual cause of death was cytotoxicity caused by excessive ion influx, similar to the excitiotoxicity observed in TBI.
So as you can imagine eating spicy foods can actually kill these neurons, desensitizing your mouth to the pain a jalapeno can produce.

I did mention a pharmacological importance that is briefly covered by the authors, although they do not go into any sort of detail about it. In the opening paragraph they say that this nociceptor desensitization has lead to use of capsaicin as an analgesic agent in the treatment of n analgesic agent in the treatment of disorders ranging from viral and diabetic neuropathies to rheumatoid arthritis. While they do not elaborate on the mechanisms of this we can assume that these diseases cause pain through stimulation of these same nociceptors.
Posted by      Zach I. at 2:03 PM MDT
  Christina Uhlir  says:

I am curious as to whether or not there was a discussion about the clinical uses of different peppers based on their Scoville scale heat, and the fact that they could induce excitotoxicity.
Posted on Sun, 23 Oct 2011 6:04 PM MDT by Christina U.

True or False: Emotions and Electrons Are Alike (Answer: true)

Remember that one time your girlfriend or boyfriend got ketchup on their nose while eating French fries and you thought it was hilarious, but immediately afterwards you felt guilty because they glared at you and growled for a napkin?

There is a word for that: ambivalence. The word ambivalence means that you feel two contradictory emotions (hilarity and guilty) simultaneously. Look a little more closely at the word ambivalence and you can probably guess what electrons and emotions have in common: valences. Emotional valences, like valence electrons, are shown outwardly on a persons face and they either attract (positive valence) or repel (negative valence) the person at which they are directed.

Many studies, since the advent of the fMRI, have examined the underlying circuitry involved in the expression and perception of emotion, especially negative valence emotions such as anger, sadness, and fear. The paper I analyzed is no exception to this rule: researchers from Kings College London, University College London, and the University of Zürich worked together to a) ascertain the circuitry that underlies the processing of emotionally negative facial expressions, and b) determine whether or not the amygdala is involved in the conscious processing of emotive faces. Basically, they wanted to know if our first response to facial expressions is to think or react.

In the study, a pool of 40 subjects (selected based on a range of nonspecific qualities) were shown a set of 60 faces and a corresponding number of fixation crosses (an image of a white screen on which a + is superimposed), while in an fMRI. Each of the 60 faces displayed either a neutral expression or a negative expression (anger, fear, or sadness) and the subjects used a clicker to indicate whether the face did or did not show an emotion. For each face, the response time and accuracy was recorded and was used in concert with the data provided by the fMRI images. In addition to the tests performed using the fMRI, a battery of statistical tests corrected for noise and anatomical dissimilarities among participants.

The findings are significant: the amygdala is not the only cranial structure that modulates facial processing. To be more specific, their results show that while the amygdala is involved in the processing of facial affect(Dima et al 1) there are also pathways to and from the fusiform gyrus, the inferior occipital gyrus, and the ventrolateral prefrontal cortex, which do not involve the amygdala. Most notably, anger was mediated by the inferior occipital gyrus and ventrolateral prefrontal cortex, not the amygdala.

What does all of that mean?

Basically, our brains have evolved for cognition for so long that we now respond to physical or emotional danger (anger in this case) in a cognitive fashion. We think before we react to a potentially harmful event.

Now think back for a second to your girlfriend or boyfriend with ketchup all over their nose. If this research holds, you will not immediately react and give them the napkin; you will, in fact, think about the potential harm that could come to you if you do not (minimal: they probably will not punch you), and the potential benefits you will reap if you do not (photographic evidence of the event). As far as I am concerned this decision is easy: memory is leaky; emotions are transient; but a picture lasts a lifetime.

What would you do?

Edited by      Christina U. at 2:03 PM MDT
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Z is for Zinc

Zinc. Metal. Number 30 on the periodic table. Twenty-fourth most abundant element on Earth. Common oxidation state of 2+.

Did you take your multivitamin today? Did it have zinc in it? Zinc is used to treat a wide variety of ailments from acne to the common cold, but did you also know it's important in memory formation? A new study lead by James McNamara M.D. of Duke University Medical Center shows that zinc can enhance communication between cells, particularly in the hippocampus, a center of memory formation. This data leads to the hypothesis that excessive enhancement mediated by zinc might occur in epilepsy and play a part in the severity of seizures. These findings could lead to developing new drugs for epilepsy.

High concentrations of zinc in synaptic vesicles was discovered in the 1950s and has perplexed neurobiologist ever since. These vesicles are colocalized with glutamatergic neurons of the hippocampus suggesting that zinc might be released and play a role in the plasticity of excitatory synapses. Efforts to determine zinc's function in these synapses has been difficult to determine because of previously available zinc chelators which were not specific for zinc and did not bind fast enough to remove zinc in the time scale of synaptic transmission. In the September issue of Neuron, a collaboration between Steve Lippard from MIT's Department of Chemistry and Duke University Medical Center has synthesized a novel zinc chelator. By using the chelator in mice, they found that zinc promotes presynaptic and inhibits postsynaptic long-term potentiaion in the mossy fiber-CA3 synapse.

The group began by creating a new zinc chelator, called ZX1, that binds zinc fast and has a higher specificity for zinc versus calcium or magnesium than other chelators. By using ZX1 to remove zinc from the synapse as soon as it was released, they were able to look at what happens to long-term potentiation without zinc. Using ZX1 in the hippocampus of mice, the data found that ZX1 inhibited mossy fiber-LTP. Mossy fiber LTP is NMDA independent, working by other mechanisms based in the presynaptic cell. The group also did experiments on ZnT3 null mutant mice, which lack the transporter that packages zinc into vesicles. These experiments were surprising because they saw that, as previously seen in wild type mice, zinc enhanced the presynaptic mf-LTP, but zinc actually inhibited postsynaptic mf-LTP.

Overall, zinc seems to modify the circuits related to learning and memory, but don't start gobbling down zinc supplements just yet. Zinc is a trace metal in biology, and certainly too much can be toxic. Knowing the molecular mechanisms of synaptic plasticity and excitability is an important step in treating diseases such as epilepsy, but as of yet there is no established beneficial level of zinc. In fact, too much zinc might increase the enhancement of these synapses, leading to more severe seizures. A new drug might act like ZX1 to bind zinc and remove it from the synapse, in order to reduce the enhancement of the excitatory synapse.

Enhui Pan, Xiao-an Zhang, Zhen Huang, Artur Krezel, Min Zhao, Christine E. Tinberg, Stephen J. Lippard, James O. McNamara, Vesicular Zinc Promotes Presynaptic and Inhibits Postsynaptic Long-Term Potentiation of Mossy Fiber-CA3 Synapse, Neuron, Volume 71, Issue 6, 22 September 2011, Pages 1116-1126, ISSN 0896-6273, 10.1016/j.neuron.2011.07.019.

Less in depth summary of paper:
Posted by      Amanda W. at 1:35 PM MDT
  Christina Uhlir  says:

Did the article actually get into how much zinc you should consume on a daily, weekly, or monthly basis? Or how much could kill a person?
Posted on Sun, 23 Oct 2011 8:37 PM MDT by Christina U.
  Amanda Weaver  says:
No, the study was focused on mouse hippocampal slices and was not advocating zinc supplements in humans, nor exploring the possible benefits or dangers inherent in changing zinc levels. In fact zinc can definitely be harmful. Here is a very interesting case study that was printed in the New York Times:
Posted on Mon, 24 Oct 2011 12:37 PM MDT by Amanda W.
  Christina Uhlir  says:
That article was certainly illuminating. I guess I am glad that my vitamins do not contain even trace amounts of zinc.
Posted on Mon, 24 Oct 2011 3:27 PM MDT by Christina U.

The Better to Remember You With, My Dear...

We've all heard those reports on "super fruit" or the next magical food to prevent this disease or to cure that disease during slow news days. While these stories are lovely fluff pieces, they often lack substantial support. Fortunately, a group of neuroscientists took it upon themselves to perform a legitimate study and to pull information from reliable research in order to identify certain foods that may be helpful in fighting the curse of aging, as well as pinpoint the beneficial effects of these dietary components.

The studies revolved around prevention and possible therapeutic techniques for neurodegenerative diseases and the aging of the brain in general. The first substance of focus was polyphenol, found most often in berry fruits. During experimentation on rat subjects, there proved to be a significant improvement in motor abilities in the group receiving a diet rich in polyphenol while the abilities of the control group either
deteriorated or maintained. In the experimental group, there was also an improvement in various aspects of memory, including LTP, fear conditioning, and both hippocampal-dependent and striatum-dependent memory. It is believed that the reasons for these enhancements are not only the antioxidant activity of the fruit, but also the positive effects on neuronal communication, a neuron's ability to buffer against calcium, and lessening of stress signals. Polyunsaturated fatty acids found mainly in walnuts have been found to improve age related motor and cognitive declines, too.

The article makes it clear that two important factors of the negative effects of aging are oxidative stressors and inflammatory issues. While not much is known about the specific mechanisms that these compounds work on, it is inferred that one of the reasons that they are so beneficial is because of their ability to reduce oxidative stress. Oxidative stress could cause disruptions in the balance of cellular calcium and could cause issues in neuronal signaling. Furthermore, high levels of oxidative stress can ultimately cause gene expression to be changed which could have drastic effects on the dynamics of individual cells, as well as the function and interaction of large groups of neurons. Docosahaenoic acid, or DHA, contained in walnuts and fish oil also plays a large role in the positive activities of these foods. DHA has been linked to anti-inflammatory properties that work to prevent Alzheimer's Disease. It seems that DHA is able to reduce Aβ oligomer production which in turn reduces toxicity levels within cells.

The disadvantages of the use of these foods are heavily outweighed by the advantages. The principal disadvantage stated in the article is the fact that relying on these foods to prevent neurodegenerative diseases could be hard to stick to because of the lack of variety. That is obviously dwarfed by the advantages brought up in the study, a few of the obvious being "safety, broad spectrum utility, low cost, and suitability for prevention." Giving up variety in order to delay ailments such as Alzheimer's Disease and Parkinson's Disease is a minor drawback.


Joseph, James, et. al. Nutrition, Brain Aging, and Neurodegeneration. The Journal of Neuroscience. 29(41): 12795-12801. < >
Posted by      Breanna S. at 12:19 PM MDT
  Christina Uhlir  says:
So sweet, and not just the fruit. But thank you for posting such an uplifting blog, sometimes it's easy to forget about all of the advances in light of all the studies that have negative or inconclusive results.
Posted on Mon, 24 Oct 2011 6:20 PM MDT by Christina U.
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Neurotheology - This is Your Brain on God

Since the dawn of the human species, mankind has maintained a belief in some form of spirituality, of God or Gods and an afterlife. Are we wired to believe in "something greater" than ourselves? Why are some people more likely to believe - to take leap of faith without question - while others resist, blocked by logic and control? What happens to us physically during these moments of spirituality?

Studies in a relatively new neuroscience field dubbed "neurotheology" are exploring the connection between our brains and God.

Neurologist Vilaynur S. Ramachandran explored a long-standing correlation between temporal lobe epilepsy and religious fervor. He asked some of his epilepsy patients to listen to a variety of neutral, sexual, and religious words while measuring brain activity and found that religious words such as "God" elicited a higher emotional response, indicating that people with this type of epilepsy have a greater affinity for spiritual experience. The temporal lobe was found to be a sort of "god spot" in the brain.

Researcher Michael Persinger took this a step further by creating the "God Helmet" which focuses weak electromagnetic fields on specific areas of the brain's temporal lobe eliciting feelings commonly attributed to spiritual experience. Persinger asserted that spiritual experience is merely the result of electromagnetic activity in specific areas of the brain.

Using Single Photon Emission Computed Tomography (SPECT), leading neurotheology researcher Andrew B. Newberg and his colleagues have taken a peek at the brain areas that are activated during prayer and meditation. Buddhist monks showed decreased activity in a portion of the parietal lobe and increased activity in the right prefrontal cortex. Newberg explained that the lowered activity in the parietal lobe could explain the monks reported feelings of being at one with the universe when meditating while the enhanced activity in the prefrontal cortex was associated with intense concentration.

Quebec neuroscientist Mario Beauregard believes that there is no single "god spot in the brain" or even a few "god spots" as Newberg suggests, but rather a complex network is involved in spiritual experience. To test his theory, he used functional magnetic resonance imaging (fMRI) to study the brains of nuns while they altered between religious and control states. He discovered six regions to be involved including increased activity in the caudate nucleus (possibly involved in the nuns' feeling of love for God), neural sparks in the insula (could be associated with pleasurable feelings felt), augmented activity in the inferior parietal lobe(oddly the opposite of Newberg's findings), and other regions involved to a lesser extent were the medial orbitofrontal cortex, the medial prefrontal cortex, and the medial temporal lobe.

In order to further test his hypothesis, Beauregard decided to use a faster technique called electroencephalography (EEG). Using this technique, Beauregard reported lower-frequency waves in the parietal cortexes and temporal lobe associated with a trance-like state.

While such research will never be able to prove or disprove the existence of a God, it may lead to a better understanding of the neural activity associated with human religiosity and spirituality-- why we believe.

Main article:
Biello, D., (2007). Searching for God in the Brain. Scientific American Mind, 18, 5.

Further Reading:
Neural Correlates of a mystical Experience in carmelite Nuns. M. Beauregard and V. Paquette in Neuroscience Letters, Vol. 405, No. 3, pg. 186-190; Sept. 25, 2006

Why We Beleive What We Believe. A. Newberg and M. Robert Waldman. Free Press, 2006

The Spiritual Brain. M. beuregard and D. O'Leary. harperCollins, 2007.
Posted by      Samantha H. at 9:49 AM MDT
Tags: religion
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  Christina Uhlir  says:
Aren't there myriad confounds with trying to broadly categorize religion, mainly stemming from the fact that there are a variety of religions and the manner in which each religion addresses god(s) and goddesses, prayer, and devotion? Why not address each religion as its own entity, rather than lumping them all together?
Posted on Mon, 24 Oct 2011 7:33 PM MDT by Christina U.
  Samantha Humann  says:
I think most scientists due. But what is really interesting, is that many diverse religions with their own diverse forms of practice are showing many of the same results in the brain. But you are correct. Spirituality is extremely difficult to difine even within one religion.

For example in Christianity (the dominant religion in the United States), there are many diverse forms of practice. Religious practices have been difficult to measure because while prayer is reported as almost universal in the United States, the actions, beliefs and commitment of those who partake varies dramatically. For example, while the majority of Americans claim to pray daily, the type, purpose and intensity of such prayer is not consistent. While some may offer a daily prayer of thanksgiving before a meal, others may engage in intensive prayer. Similarly, regular church attendees may do so for diverse reasons. Studies have used various methods to identify participants in prayer research ?? from single scales such as reported frequency of prayer and regular church attendance to devotees?? perceptions of God as remote or intimate to most recently, using multidimensional measures which include behavioral, social, psychological pathways to religiousness and spirituality. In addition, research has often focused on participants from a specific Christian denomination. The lack of a clearly defined participant selection for studies on the mental health benefits of prayer combined with reported individual religious experiences complicates and, at times, dilutes the data on the benefits of prayer to mental health.

Social responses to Neurotheology differ greatly.
Posted on Wed, 26 Oct 2011 7:56 AM MDT by Samantha H.
  Christina Uhlir  says:
Do you have any running theories as to why a) scientists tend to generalize their results about religious studies and b) why the results can be translated from religion to religion? And for that matter, why research would focus on Christianity in particular?
Posted on Wed, 26 Oct 2011 7:33 PM MDT by Christina U.

October 22, 2011

Sleep and spines modulate your mind...and your brain?

"The mind is the brain doing its job." - Simon LeVay, 1994

We know that sleep is good for us: it's a daily, regularly- or irregularly-scheduled body and brain maintenance check. The sleep/wake cycle maintenance staff in particular is profoundly important in synaptic renormalization (homeostasis) by modulating (decreasing) synaptic size and/or strength in the adult brain. In the adult brain; surprisingly, this doesn't exactly hold for the adolescent brain, where sleep/wake cycle maintenance staff is responsible for more synaptogenesis (synaptic formation) and synaptic pruning (synaptic elimination).

A recent article published in Nature Neuroscience examined the process of cortical development (that involves synaptogenesis and pruning) in adolescent YFP-mice (through two-photon microscopy) as a function of different sleep/wake cycles: W1S2 mice (wake followed by sleep), and S1W2 mice (sleep first followed by wake). Mice were allowed to sleep or kept awake for each behavioral state (sleep/wake) for durations that mimic physiological sleep/wake cycles (6-8 h) and then imaged. Interestingly enough, they found overall decreased spine density in W1S2 mice and increased spine density in S1W2 mice; there was no variation observed in mice in early or late adolescence. Waking results in a net increase in cortical spines, and sleep is associated with net spine loss.
A third experimental group of W1SD2 mice (wake followed by sleep deprivation), to control for decreased spine density as a function of the passage of time showed a net increase in synaptic density.

In summary:
Wake followed by sleep (W1S2) = spine loss
Sleep followed by wake (S1W2) = spine gain
Wake followed by sleep deprivation (W1SD2) = spine gain

Sleep might actually be bad! (...for dendritic spines, that is)

The wake-sleep deprived group presents an interesting case. Sleep-deprivation, akin to pulling an all-nighter, shows a net increase in spine density. Therefore, sleep deprivation is one way to keep your dendritic spine density (that is, until you crash of exhaustion). Sleeping for the recommended 8 hours a night is also a default option. For those of us in adolescence, retaining spine density though sleep-deprivation is still theoretically a viable option. A different experiment conducted by the same researchers imaged the mice after 2-3 hours of sleep (short sleep) or wake (short wake). Both groups showed no net changes after short sleep or short waking. It may be theoretically possible to maintain spine density through a sleep-deprivation following wake with short sleep sleep/wake cycle (power naps anyone?).

This article concludes by suggesting that behavioral state modulates spine turnover in a manner consistent with the need for synaptic homeostasis; in the adult brain this translates into synaptic renormalization, and in the adolescent brain (regardless of exact developmental stage of adolescence) this translates into synaptogenesis and synaptic pruning. Sleep may therefore facilitate spine elimination or spine loss in certain phases of development. Sleep deprivation during adolescence may affect synaptic turnover, as it blocks sleep-related spine pruning; however, it does not result in a further increase in spine density. It is currently unclear to what extent the role of sleep in spine elimination is permissive and/or instructive.

So what does sleep and spine density have to do with anything? In the adult brain, it decreases synaptic size and/or strength; in the adolescent brain, it modulates synaptic pruning during a period of massive synaptic remodeling. Synaptic spine density is a part of how the brain does its job. Spine density therefore affects the mind (the brain doing its job that feeds to the mind). Changes in our minds are therefore a result of the brain doing its job differently, and how the brain does its job differently can involve changes in synaptic spine density. Spine density subsequently affects the different jobs of the brain; spine density affects the mind. Sleep (the sleep/wake cycle), therefore, is especially critical in cortical development during adolescence in modulating synaptic spine density (long-term potentiation anyone?)

I should probably get more sleep myself...

Posted by      Patricia W. at 10:19 PM MDT
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Meditation: New Discoveries of Old Traditions

It isn't often in science that old methods of treatment are re-centered from their otherwise un-scientific past, to present as one of the more progressively favored treatments in modern society. However, it seems as though the old practice of meditation is working to accomplish just that. Chronic pain sufferers have endlessly struggled to find methods of treatment that they are not resistant to, or that their pain does not overcome at some point. Perhaps in favor of a reduction of cost and a more "natural" method of healing, meditation was further studied--and these studies are proving most beneficial. Research has shown that by practicing a state of "mindfulness", one can achieve decreased overall pain, as well as pain intensity.

Such mindful "interventions" have aided our understanding of pain disorders (both acute and chronic). With extensive training of one's mind (meditation), it is found that one's cortical regions that are associated with pain are thickened, perhaps enhancing that persons perception of their pain. This results in changes in their normal evaluation and perception of pain. These effects of mental training can result in a more beneficial method of neuroplasticity.

But how exactly does one measure pain? Surely we do not expose trial studies of non-pain sufferers to painful stimulus in order to further science! Why of course not--in fact, what is generally used in pain studies is not in fact 'pain' at all. Experiments with temperature extremes (hot and cold) are used to test the participant's perception, durability, and sensation of a 'painful' stimulus. In a particular experiment adhering to the purpose at hand, they tested the unpleasantness of the stimulus (hot water) before and after a series of meditative exercises. However, rather than test the person's personal opinion of the pain, they tested the person's brain's perception of the pain through measurements of Cerebral Spinal Fluid, through a method called ASL. ASL is an "MRI pulse sequence that provides a measure of CBF using water as a flow tracer". Using ASL, they found OFC (orbitofrontal cortex) activation, and deactivation of the thalamus. During painful stimulus, usually the opposite occurs--a decrease in OFC and an increase in thalamus activation are seen. This study concluded that short term mediation can decrease the affect pain, and the experience that goes along with it.

It is important to take this discussion with a grain of salt. Even though these studies did work, I believe it is essential to define the term "meditation". Perhaps all it encompasses is distraction from temporary pain, having your mind focused on other things, thus rendering it less activated in the pain 'areas' of the brain. This type of treatment would not necessarily work for those who are suffering chronic pain. However, I feel more work in the field of long term mindful trainings may prove beneficial to act as a sole treatment or a combination treatment to pain disorders.

Another limitation to this experiment is the role of an adequate control group. I felt that they had no data to argue their finding against. The perception of the irritating stimulus may have simply decreased because they had already experience it once, and could therefore were more comfortable experiencing it again. It is crucial to create a group that simply received both tests without any meditation, to see what the conclusion of diminished pain was really measuring. Nevertheless, to whatever degree this breakthrough is effective, one conclusion is for sure--studying mediation and perception of pain enables us to further understand just how our brain handles painful or noxious stimulus. Hopefully we are able to use such methods of research (such as ASL) in order to provide helpful, more affordable treatment for the individuals suffering from pain disorders.

Posted by      Amber S. at 5:15 PM MDT
  Christina Uhlir  says:

This is lovely! My mom had postherpetic neuralgia and japanese accupuncture actually worked wonders for her.
Posted on Sun, 23 Oct 2011 7:46 PM MDT by Christina U.
  Emily Nelson  says:
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October 21, 2011

A Mechanism of Auditory Processing

Ever wondered how you're able to distinguish between different sounds and words in conversation? In order to understand the world around you, you not only have to hear all of the sounds together, but you also have to be able to hear the silence between the sounds. But all of this has to occur very quickly, or else you would be stuck having people repeat themselves slowly every time they said something. So, how does it work? The answer is: rapid changes in concentration of ions from cells that are firing electrical signals and turning off.

Previous research has implicated two structures in the brain that are critical in recognizing sounds and silences, namely the superior paraolivary nucleus (SPN, sometimes spelled superior periolivary nucleus) and the medial nucleus of trapezoid body (MNTB), both of which are part of the superior olive in the brainstem. A more current research article ("The Sound of Silence: Ionic Mechanisms Encoding Sound Termination" by Kopp-Scheinpflug, et al.) looks at how these two structures connect to one another and what mechanisms they use for distinguishing sounds.

In general, when a neuron is not being activated, it sends electrical signals at a specific rate, called its basal firing rate. Stimulation can increase or decrease the neuron's firing, and when the stimulation is removed, the firing rate eventually returns to its basal level.

When a sound stimulus is presented, the MNTB neurons continuously fire for the entire stimulation, and then not only cease firing when the stimulation has ended, but also reduce firing to below their normal rate, and return back to normal after a short period of time. On the other hand, SPN neurons have little to no firing when a sound stimulus is presented, and when it stops, the neurons rapidly fire, corresponding to the intensity of the stimulus and then deplete the firing to their normal rate.

The signaling pathways for both SPN and MNTB also involve chloride ions (and possibly potassium ions). The flow of chloride ions into neurons inhibits firing, and is important for recognizing sound in the MNTB, but recognizing silence in the SPN.

The main idea here is that there are multiple mechanisms involved in how we process language and other sounds every day. Without these two brain regions and the chloride signaling between them, we wouldn't be able to communicate. It is necessary to have mechanisms in our brains not only for recognizing sound, but also for recognizing silence, both of which need to communicate with one another to be processed together. This is a very important finding for learning how we acquire language and learn to differentiate syllables and words so readily and easily in early childhood, and more research could possibly help with understanding different speech disorders.

Posted by      Anna G. at 10:54 PM MDT
  Christina Uhlir  says:

Thank you for spelling it out so simply, I understood that we process continuous sounds as discrete but I couldn't understand how that was accomplished, so thank you for elucidating that point for me.
Posted on Sun, 23 Oct 2011 7:44 PM MDT by Christina U.
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October 20, 2011

The Placebo Effect...Does it work?

Ever since 1978, scientists and researchers have been studying a psychobiological phenomenon known as the Placebo Effect. The Placebo Effect is used to study the psychosocial context that affects the therapeutic outcome of any medication. In order to do this, you must eliminate the effects of a given drug and stimulate a setting that is similar in all aspects to that of the real treatment, a sham experiment. This phenomenon is important in our understanding of the roles that expectations and conditioning can have on our brains, as well as creating a model to understand how mental activity interacts with our neuronal systems.

Although the Placebo Effect can broaden our conception of the human capability, and give us an idea on how beliefs and values shape our brains, it can also have some clinical and ethical implications. The use of placebo bills on patients during clinical trials with the presence of effective treatments has raised many ethical controversies.

The paper, "Neurobiological Mechanisms of the Placebo Effect", from the Journal of Neuroscience has provided many different studies to understand the mechanism of the Placebo Effect.

Parkinsons Disease has been used as a model to understand this Effect. A study found that placebo-induced expectations of motor improvement activate Dopamine in the striatum of Parkinsonian Patients. It was also found that the expectations of good versus bad motor performance regulate the therapeutic effects of subthalamic nucleus stimulation in Parkinsonian patients. Analyzing the velocity of the right hand movements in response to a subthalamic stimulation was faster when patients expected a good motor performance suggesting that expectations stimulate neural changes very rapidly.

A study that was done found that the personality of a person had an effect on the success of a placebo as well. Individuals who were more optimistic are important contributors to the Placebo Effect. On the other hand, individuals who had poor responses to previous treatments showed lower placebo responses due to negative expectations and conditioning.

The neurobiological effect of the placebo was also studied in individuals suffering from major depression. A PET study measuring the cerebral glucose metabolism was done using FDG and regional CBF since they have been found to be sensitive to brain function in untreated depressed patients and after treatments. After various treatments, many corresponding changes in brain areas were identified, causing these specific effects to be consistent with the hypothesis that different interventions regulate specific targets. This neural architecture then provided a foundation in studying the Placebo Effect under similar and comparable conditions, and the following hypothesis was created, "if expectation and conditioning are the principle mediators of such effects, one would predict comparable patterns between active and sham-treated responders in a given experiment, if pathways mediating expectation and conditioned learning are not otherwise impaired." The study findings suggests that placebo changes are very unlikely related to passive psychotherapy effects, and instead, they are related to specific effects of expectations and conditioning facilitated by the psychosocial context of the trial.

As you can see, theres still a lot to be explained from the phenomenon of the Placebo Effect, however, as more information is gathered, we are getting a much better understanding of the human self-regulatory system, and with time, we will only become experts and masters of the capability of the human brain.
Posted by      Nawal E. at 8:59 PM MDT
  Christina Uhlir  says:

Could you explain what FDG and CBF are? I'm not familiar with those acronyms.
Posted on Sun, 23 Oct 2011 2:32 PM MDT by Christina U.
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Neuro-education... the Key to Education Reform?

Any American who has attended a public school has likely walked out of a classroom having no idea what that boring, Charlie Brown-esque (Blah, Blah, Blah, Blah, Blah), lecture they just listened to was about. But, just as many people likely have stories of those one or two miraculous teachers who inspired them to learn and to think in new, innovative and creative ways. What is it that makes some lessons incredibly ineffective and others amazingly stimulating?
The emerging field of Neuro-education is hoping to find the answer to this question and many others concerning the most effective ways to teach the world's kids. Neuroscientists and educators are working in collaboration to blend findings in both fields to better understand how humans learn in order to develop more effective educational methods and policies. New programs are opening up in the U.S., and throughout the world, that are hoping to develop connections between disciplines in order to create a better educational system for our kids. One such organization, the International, Mind, Brain and Education Society states its mission, to facilitate cross-cultural collaboration in biology, education and the cognitive and developmental sciences in order to bring science and practice together.( Many graduate programs at universities ranging from Cambridge's science based "Centre for Neuroscience In Education" ( to Johns-Hopkins School of Education's "Neuro Education Initiative"( have been formed with similar mission statements.
The ideas behind these programs and this field are innovative and logical. The goal of scientific research in Neuroscience is to better understand how the brain works. The goal of education is to help the brain work to its best potential. Combined, these fields can provide groundbreaking ideas to change and improve how kids learn. In the US, many people believe that the public education system is failing kids, thereby lowering the prospects for this country's future. Between budget cuts and outmoded and unsuccessful teaching methods, people are calling for reform. But one central question is: how should we reform and what direction should it take? Neuro-education has the potential to provide the evidence on the science end and the experience on the educators end to form and shape education reform.
So, what is necessary to make this happen? First of all, like everything involved in education, it needs more funding. From the university to the federal government level, funding must be provided in order to promote new research, to integrate findings from multiple fields, and to implement new ideas into the classroom. Currently, less than .5% of all educational funding goes to research. The prospects of this changing in the current economic climate, where schools are struggling just to buy books for the classroom and keep class sizes at a reasonable level, seems slim.
Secondly, and perhaps most importantly, the lines of communication need to be opened between researchers in scientific fields and the people who are directly involved in the education of kids. This means that research findings must be presented in forms that are accessible to busy parents and teachers. Already, Neuroscience has developed an extensive body of knowledge about areas of high importance to education. The effects of sleep, stress, exercise and musical training on memory retrieval and learning consolidation are already well understood. Our country and public education system must find a way to get these finding to educators so that they may be translated into real practice.
In order to give kids the best prospects for their futures, and thereby, the best prospects for our country, the ultimate goal of education should be to inspire kids and imbue in them a sense of curiosity, creativity and competition. This combination between a scientific understanding of the brain and educational reform has a real and exciting potential to make a difference in the futures of our kids and our country.

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Posted by      Megan M. at 10:18 AM MDT
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Can we trust Neuroscientists?

October 19, 2011

Typically, neuroscientists, or among all scientists, fail to provide full disclosure of the project to a participant in order to obtain valid knowledge on the phenomena being investigated. Although this methodology is widely used by many scientists, it however proves to be an ethically controversial topic. The idea of deception in human experimentation becomes unethical as the informed consent required by the individual is not completely transparent of the research, thus lacks a degree of respect for the persons utilized in the experiment. Hence, how can the vast majority of psychology and neuroscience projects be approved by ethic committees if deception is a common methodological theme? Are participants rights triumphed by the knowledge gained by the experimentation? To what extent are unethical methods permitted by ethic committees and what makes one idea allowed and another not? These are questions that we should be asking ourselves, knowing that science should not be independent of ethical and moral values.

It comes to my attention that a capacious amount of published articles using deception as a method to obtain valid knowledge by the participant is not specifically stated so in the journal article. Without blatantly stating that this form of research utilized deception, a person that is unaware of ethical issues within research may not realize that some participants were not given proper information.

Understandably, deception in research is a methodology that is not going to leave science any time soon. Therefore, it is necessary to make it prevalent to the public that this occurs and for readers of the research articles to be fully aware of the use of deception. I believe that it is pertinent that if a researcher decides to integrate deception into the procedure, it should be clearly stated within the Materials and Methods section of the journal article. Overall, I believe that the nature of the research should be explained to the participates after the experimentation, such that it will soften the overarching ethical dilemma. This may ultimately limit the participant pool, but it does give a degree of respect from the researcher to the participants that is truly deserved.

Personally, I believe that it is our right and our duty, as readers and future neuroscientists, to take this matter seriously. We should not allow researchers to infringe upon participants rights to be tested when there is a lacking of transparency of the nature of the research. We should encourage our colleagues and higher authorities to demand that experimental deception included in the research should be explicitly stated within published articles and individuals be debriefed of the entirety of the project. Adding these boundaries to published articles will not only provide a more ethically sound publication, but will promote respect for science among readers that are not familiar with the field when full disclosure of the experimentation is available to the public eye.

Original article:
Posted by      Sarah H. at 12:16 AM MDT
  Christina Uhlir  says:

Objectively speaking, would you or wouldn't you trust a neuroscientist?
Posted on Sun, 23 Oct 2011 2:23 PM MDT by Christina U.
  Sarah Ha  says:
Personally, I wouldn't want to be a participant in an experiment if I'm not given full disclosure of the purpose of the experiment. Plus, it makes me more skeptical when I read journal articles of overall results if the published article is fully disclosing their methodology. How can I repeat their experiment if I don't know exactly what they did?
Posted on Tue, 29 Nov 2011 3:56 PM MST by Sarah H.
  Nathan Jones  says:
Trust can sometimes be subjective. Though, in my opinion, yes - we can trust neuroscientists. Their job is not simple and it's not easy to study the human brain. They do their best to provide solutions and discover new things relevant to society. corporate law firms Sydney
Posted on Mon, 9 Mar 2020 9:41 PM MDT by Nathan J.

October 19, 2011

Well that's Negative

Have you ever been surprised to be let down? Or in other words, have you ever expected a certain outcome only to be surprisingly disappointed? Well if you have, ladies and gentlemen, then do not fear; for your dorsal anterior cingulate cortex is functioning properly! And what's that? There's unified model for the long disputed function of the dorsal anterior cingulate cortex? That's right! Both of these birds were hit by the same stone recently when Alexander and Brown produced a computational model "tour de force" to illustrate how negative surprise signals drive dACC (dorsal anterior cingulate cortex) and mPFC (medial prefrontal cortex) responses.
Many theories have been concocted as to what the dorsal anterior cingulate cortex may be responsible for, such as error detection, error likelihood prediction, and conflict monitoring primarily, and even more such as reinforcement-guided decision making, negative reinforcement learning signals, and action value prediction error. Could the dACC be responsible for all of this in the brain? Well, Alexander and Brown's model seems to narrow our spectrum a bit and put an end to this controversy.
While their model agrees with previous theories that the dACC and mPFC predict action-outcome situations, it is uniformly different in the sense that these regions are responsible for multiple predictions for action-outcome situations in parallel, and then these predictions are scaled to their probability of their occurrence. When the predicted outcome doesn't happen, learning rates are modified in order to update action-outcome predictions to the degree necessary to learn from mistakes and find a better solution.
Another important point of this model's representation of multiple predictions of action-outcomes is that different ongoing predictions could account for heterogeneity of neural responses usually observed in single-unit studies. So basically, the dorsal anterior cingulate cortex and medial prefrontal cortex can encode different outcomes simultaneously for the same situation that are being encoded in different groups of neurons! Pretty impressive eh?
So let's just recap. The dorsal anterior cingulate cortex analyzes a particular action, predicts an outcome for this action, and if the action-outcome prediction is negated, then the dACC modifies learning rates so that the brain can learn from its mistakes. And the dACC and mPFC can do this multiple times at once!
So while Alexander and Brown's model is reasonable and presents much more concise data, it is obviously provoking new questions and controversy. Seeing as how consequences of positive and negative surprises are the same according to this new model, what makes a negative surprise more significant or important than a positive surprise? If the dorsal anterior cingulate cortex is responsible for negative surprise predictions and reactions, what is responsible for positive surprise monitoring? As for these questions, we shall see what new models of these mysterious brain regions are presented and what will be discovered for the tasks we perform in daily life. Regardless of what is discovered in the future, we'll all be surprised!

main article:
Posted by      Mark A. at 4:19 PM MDT
  Christina Uhlir  says:
Mr. Alsberg,

Could you kindly explain the mechanism by which the "tour de force" operates?
Posted on Sun, 23 Oct 2011 2:20 PM MDT by Christina U.
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