NRSC 4132 Blog

You just finished your 30 mile bike ride or just finished that triathlon you always wanted in great time.. Now your exhaustedâ?¦ now what why canâ??t you finish your thought? Is it possible that the muscle fatigued you experiences can impacted you mentally? Studies indicate that the mental and actual movements share overlapping neural substrates (Jeannerod, 2001; Fadiga and Craighero, 2004; Munzert et al., 2009) and preserve the same spatiotemporal characteristics according to Demougeot. Demougeot suggested that if the two components are related that one will have to mentally prepare or exercise the mind to have optimal performance. ..â??Appropriate mental training can enhance motor performance.â?? Demougeot seek to find the answer to have much physically activity or muscle fatigue will start to have an effect on the mental stabilization of oneâ??s cognitions? In their study they measured the temporal features of actual and mental movements before and after muscle fatigueâ?¦ â??A strong prediction is that duration of mental actions should be sensitive to muscle fatigue, because the forward model receives as input the efferent copy of inappropriate motor commands and the perturbed state of the arm, both caused by muscle fatigue.â??

To conduct their study they used seventeen adults who were all health with no neurological problems who they used as participates. The participates then were asked to move their arms, physically and then mentally at different angles in a conducted sequence. They then tested the participate before and after the muscle fatigue.

They discovered that muscle fatigue significantly influenced the mental aspect of the experiment. Demougeot discovered that muscle fatigue significantly influenced alterations in the signaling used in mental cognition. They also discovered actual movements were in general slower immediately after fatigue, but progressively returned to prefatigue values. When applied to their study they discovered that mental movements were faster immediately after fatigue and gradually returned to prefatigue values. Demougeot studied the motor effent outflow signals to justify their thesis and this is what the concluded â??However, its efferent copy is available to the forward model, which naturally predicts very fast movements. Since during mental movements there is not sensory information, and state estimation derives from forward model alone, the brain continues to simulate faster mental movements after fatigue based on inappropriate (large) neural drives. This explains why mental movements were consistently faster than actual movements after fatigue, at least until their complete adaptation. This process, i.e., state estimation without sensory feedback, also explains the slower update of motor controller (i.e., motor commands) during mental compared to actual movements after fatigue. â??

Though neuroimaging Demougeot discovered that muscle fatigue can greatly impact oneâ??s ability to mentally function as proven above. One can also conclude that next time you stay up to study all night for an exam (muscle fatigue) that it could be detrimental to our test grade. Demougeot proved that muscle fatigue influences motor performance and action planning. Itâ??s no longer enough for physically training but mentally training is required now too.

To read full article please follow https://cuvpn.colorado.edu/content/31/29/,DanaInfo=www.jneurosci.org+10712.full

Reconsolidation theory states that the reactivation of memories destabilizes them unless they are reconsolidated within a certain amount of time. A study by Susanne Diekelmann shows that memory reactivation actually serves different purposed when we are awake and when we are asleep. Apparently memory reactivation during slow wave sleep results in an immediate stabilization while reactivation during wakefulness still results in destabilization. Diekelmann and her lab reactivated memories by presenting subjects with odors, and used fMRI technology to image the brain during reactivation. Participants in this study learned during the evening in the presence of an experimental odor in order to establish a connection between the odor and the material being learned.

During slow wave sleep, the participants were presented with the odor and then awoken a few minutes later to be started learning an interference object location task. Reactivating memories using the presented odor during waking lead to a reduced ability to recall the original object location task when interference preceeded. Using the fMRI, they found that reactivation during slow wave sleep activated hippocampal and posterior cortical regions whereas reactivation during wakefulness activated activated prefrontal cortical areas. Their findings indicate that the reactivations of memory traces have opposite effects on memory during slow wave sleep and awake times.

This study makes me think about Jim Carey in Sunshine of the Spotless Mind, where he undergoes a procedure while sleeping to erase all of his memories of his ex-girlfriend. While this plot seems totally unrealistic, it may be something that will be plausible in the future. But according to this study, wouldn't it be more effective to try and erase memories while people are awake? Imagine. What would the world be like if we could selectively choose the things we want to remember and those we want to be erased from our lives? We build our personalities and choices off of previous experiences, and learn from our mistakes. If we erase our mistakes, aren't we just likely to make them again? I mean Jim Carey went looking for his ex-girlfriend again in the movie.

For more information or to read this study check out "Labile or Stable: Opposing Consequences for Memory While Reactivated during Waking and Sleep" in Nature Neuroscience.

In case you don't know what they are, throat lozenges are those chalky, powdery tablets primarily composed of zinc that you take to alleviate sore throat pain. Similar to a cough drop, they've been around for years and seem to be part of many people's remedy regimen to treat such symptoms of the common cold. Pain is one of those feelings that not many of us like to deal with or even think about. Whether you are taking aspirin, acetaminophen, or throat lozenges to manage throat pain, it is known that many options are abound in the marketplace.

Pain is an unpleasant sensory and emotional reaction that usually motivates us to seek some sort of "pain-killer." Sometimes it even gets to the point where we don't care to know or what extent we have to go to alleviate our pain--symptoms of such "pain-killers" disregarded. An extensive amount of funding and research has gone into the clinical aspects of pain management drugs including not only over-the-counter pain medications such as Tylenol and Advil, but chronic pain anesthetics with detrimental side effects. Such drug categories include neurolytic blocks, narcotics, opiates, and other analgesics. Side effects from all of these drugs, acute and severe, range from topical rashes and swelling to addiction and cardiac arrest. Holistic healing, be it through ?mind over matter? or ingesting natural antidotes, may be a way to avoid pain killers that bring severe side effects with them. According to comprehensive research involving zinc in last month's issue of Nature Neuroscience, perhaps there are some natural treatment methods of pain management.

Zinc, as previously mentioned, is a metallic chemical element that is readily available and affordable throughout the marketplace. In fact, it is so copious, that it is the 24th most abundant element in the Earth's crust, and the second most prevalent trace element in the body according to Nozaki's et al. investigation. Not only is it essential for life and crucial for cellular metabolism, but Nozaki et al. have discovered a role for zinc in brain functions such as neurological disorders and pathological pain management. The trouble with studying this element is the myriad of potential zinc targets on the molecular basis. Nozaki et al. noted that NMDA receptors are one of the potential synaptic targets for zinc effects of excitatory transmission and have key roles in both the physiology and pathology of the nervous system. Notably, these receptors contribute to pain transmission and the development of chronic pain.

As we understand, there are various subunits that comprise the NMDA receptor (NR1 and NR2 subunits). In particular, the NR2A subunit, which is widely expressed in the adult nervous system, has an intense sensitivity for extracellular zinc, or zinc taken in the body beyond endogenous levels of zinc. Using knock-in NR2A-H128S mice, they found that high affinity zinc binding to the NR2A subunit is enough to dampen NMDA receptor function in pain pathways throughout the central nervous system. Though Nozaki et al. have not found the precise location of the site where zinc diffuses in the vicinity of NMDA receptors, they did find that NMDA-dependent spinal long-term potentiation, a well-known substrate for hyperalgesia, is blocked by exogenous zinc.

This is an enormous discovery in terms of future experimentation and the potential role of the natural element zinc in place of dangerous pain-management pharmaceuticals. It's absolutely incredible to me how technology is unveiling Mother Nature's organic remedy for so many of the problems and illnesses in today's society. Not that I doubt the use of western medication and synthetic pharmaceuticals as treatment options for various illnesses, but I strongly condone taking natural elements found on this planet with a far shorter list of side effects. A lesson to consider: keep on sucking on those zinc throat lozenges when you have a sore throat!

Raw sugar. Where did it go? I don't remember the last time I actually saw one-hundred percent, real, authentic sugar on the table the last time I was seated at a restaurant. Whether it's an iced tea, coffee or whatever I'm ordering that doesn't arrive at the table sweet enough to my liking, the only quick option I have is to choose one, or many, of those artificial sweetener packets located within arms reach. One might view one of those many companies who put so much time and money into making these packets so readily available at nearly every restaurant, a small additive solution to America's obesity issue that I discussed last week. Do you want sweet and low? Equal? How about Splenda? Or maybe even Truvia. Regardless, they're all fake. And for the most part, they all satisfy our need to make not only beverages, but confections and whatever else, taste more sweet.

The molecular mechanisms involved with sweet taste and the impact of artificial sweeteners are still not completely mapped out. Before I get into some of the interesting findings in the July 11' edition of The Journal of Neuroscience, let me give you a piece of advice: next time you reach for that white ceramic square containing all those fun colors of artificial sweeteners, stop yourself before you do and ask for some real sugar--it's in your best interest.

Taste qualities can be broken down into five major categories; sweet, bitter, sour, salty, and umami. Thus far, it has clearly been identified that the family C G-protein coupled receptor Tas1R2 and Tas1R3 heterodimer mediates the primary sensory transmission process of sweet taste perception. This receptor can be stimulated by many of these diverse natural or synthetic sweet ligands and proteins.

In Bo Liu et al.'s research involving artificial sweeteners, he and his team heterogeneously expressed and functionally assessed these receptors from a squirrel monkey which belongs to the genus Samimiri of New World monkeys. Using receptor chimeras between humans and squirrel monkeys, species-dependent sweet taste differences were determined by a combination of a few specific interaction sites on the Tas1R2 and Tas1R3 receptors. Using two primary ingredients to some (aspartame and neotame), but not all, artificial sweeteners, they found that Old World monkeys but not New World monkeys are able to taste the sweet sensation of such products. In their analysis of such results it was noted that specific residues, are required to taste something sweet and that the extracellular domain of the human Tas1R2 receptor is a critical site and contains important molecular determinants for activation by aspartame and neotame. Old World monkeys (and rats) had a hydrophobic binding site on these receptors which no longer exists on the New World species.

Though Liu et al. did not go on to mention any further experimentation or draw parallels for the human population, considering their BLAST search between the primates and human samples used was a strong 89% correlation some inferences can be made. To what extent evolution of New World monkeys and rats plays a part in this de-sensitization remains unknown, however, what happened to those specific species that hasn't happened to Homo sapiens yet? Regardless of whether or not we're going to potentially lose the ability to percept aspartame and neotame in the future, artificial sweeteners are already known to be bad for human homeostasis. Even though products such as Splenda (Sucralose) and Truvia claim to be all natural and aren't involved in this research, in large quantities, artificial sweeteners can be carcinogenic and in some studies have shown to actually cause weight gain. Considering the vast research boycotting the use of such products, I think it's best to say that we should just stick to the old fashioned way of making our drinks sweeter--with pure sugar cane. Whether you like it raw or not, your sugar cane that is, it just seems to be the smarter option.

Presently, we live in a society that has become increasingly dependent of pharmaceuticals as the great panacea for our discomforts and diseases. Treatment of neurological disorders is most commonly mediated through trial and error dosing of medication. This trend has steadily increased since the 1950s with the use of antidepressants and accompanied the closing of most of America?s mental hospitals. The emphasis on personal treatment and therapy has lost ground to the administration of singular chemicals (or combinations) that alter pathways with predicted but not completely understood chemical results (due to the highly interconnected nature of these chemical pathways.) This method can work wonders, many patients with severely debilitating neurological disorders such as schizophrenia often find great relief in their treatments and are able to live without or with minimal assistance. Drugs are also often a cheaper solution to the problem (compared to high levels of therapy or institutionalization.)
Unfortunately though this practice of pharmaceutical treatment has many limits; Many antidepressants that have been prescribed over the years have been found later to increase suicidal tendencies. Some people have genetic or environmentally caused dispositions that increase or decrease the drug potency or its negative side effects. Some drugs are sought out not for curing disorders or diseases but for recreational or ability enhancing uses (like the highly prevalent the misuse of adderall among students.) Then, of course, there are disorders or injuries which impair the nervous system for which there is no known treatment or specific biochemical pathway on which to act upon. For these reasons many scientists and clinicians are using nonpharmacological treatments, especially the utilization of sensory input, to help ease and heal their patients.
A great leader in this movement towards alternative forms treatment is Dr. V. S. Ramachandran. Dr. Ramachandran is a neuroscientist at the University of California San Diego and has helped people suffering with a strange neurological disorder known as phantom limb syndrome without surgery or drugs. Phantom limb syndrome is the experience of feeling of the presence of an amputated limb, it can be quite painful and is believed to be caused by lack of feedback inhibition (the brain tells the missing hand to clench but the hand cannot clench so the brain tells the hand to clench harder etc.) By using a ?mirror box? Ramachadran has found that he can use external sensory input (the patient ?seeing? his missing hand clench by using the reflection of his present hand) to override the jammed signal.
Another example of novel drug-free therapies has been the use of electrodes to serve as external sensory devices in both the treatment of vestibular malfunction and to return sight to the blind. A grid of electrodes is used in both cases and can be used as a sort of balancing meter for vestibular treatment or as a sort of low resolution black and white television (with an on electrode being white and an off electrode being black.) These treatments have shown success for many patients and may become more popular as technology advances.
These exciting and alternative therapies are of course limited, but may open the door to other forms of treatment for difficult to medicate neurological disorders.

Have you ever experienced a ?gut feeling?? Gut feelings are also known as intuitions. I?m sure you?ve all hear about your mother?s intuition? if not ? I?m sure she?ll tell you ?Mother knows best!? We all know things that weren?t taught to us?but we still know them. For example, best friend says she?s ?okay? but you know she isn?t or your newborn is sick. A gut feeling is a sudden, unexplained judgment where we don?t know the source of origin.

Science has started to research how the stomach and brain are interconnected. ?The concept that the gut and the brain are closely connected, and that this interaction plays an important part not only in gastrointestinal function but also in certain feeling states and in intuitive decision making, is deeply rooted in our language.?(Mayer, 2011)

In the August issue of Nature Review Neuroscience, the article ?Gut feelings: the emerging biology of gut?brain communication,? talks about the foundation of why there are such feelings and the pathways that are taken to create those feelings. ?Recent neurobiological insights into this gut?brain crosstalk have revealed a complex, bidirectional communication system that not only ensures the proper maintenance of gastrointestinal homeostasis and digestion but is likely to have multiple effects on affect, motivation and higher cognitive functions, including intuitive decision making.?(Mayer, 2011) The article discusses the enteric nervous system and the signaling pathways that the gut and brain used to communicate ??The brain communicates to the viscera, including the gastrointestinal tract, through multiple parallel pathways, including the two branches of the autonomic nervous system (ANS), the hypothalamic?pituitary?adrenal (HPA) axis and the sympatho?adrenal axis (modulating the gut-associated lymphoid tissue), and descending monoaminergic pathways (modulating gain of spinal reflexes and dorsal horn excitability). ? (Mayer, 2011) The article then discuss the effect of the stomach to the brain. Most of the consciously perceived information about the stomach is that it?s used for digestion?this isn?t new information. ?However, recent evidence suggests that various forms of subliminal interoceptive inputs from the gut, including those generated by intestinal microbes, may influence memory formation, emotional arousal and affective behaviours.? (Mayer, 2011)

So why do we make decision based off no information but off our ?gut feelings?? Mayer suggests that we have some ?neurological basis? when it comes to our gut-interactions. She suggests that our gut feeling based decision is due to an interoceptive map of gut responses that develops in infancy and continues to develop throughout our stages of life.

The future holds new research on the crosstalk between the stomach and the brain. The primary focus is the mapping associated with the two. ?This includes the remarkable success in mapping the functional neuroanatomy of the ENS, in our understanding of how the brain modulates these ENS circuits and gut functions, and in unraveling the complexity of gut to brain signaling through multiple parallel but interacting communication channels.? (Mayer, 2011) With our current advances in the study of gut feelings we still have many unanswered questions? stay tuned for what science discover next.
To read full article, please visit https://cuvpn.colorado.edu/nrn/journal/v12/n8/full/,DanaInfo=www.nature.com+nrn3071.html

How effective is your caffeine in the morning?
"Caffeine, a widely consumed adenosine A1 and A2A receptor antagonist, is valued as a psychostimulant, but it is also anxiogenic. An association between a variant within the ADORA2A gene (rs5751876) and caffeine-induced anxiety has been reported for individuals who habitually consume little caffeine." How many cups do you drink in the morning before you feel like you are ready to take on the day? The average intake of caffeine is on average was 346 mg per day (equivalent to about three cups of ground coffee per day). What if I were to tell you that the coffee you are drinking scientifically isn?t helping that fatigue. "Although frequent consumers feel alerted by caffeine, especially by their morning tea, coffee, or other caffeine-containing drink, evidence suggests that this is actually merely the reversal of the fatiguing effects of acute caffeine withdrawal (James and Rogers, 2005; Sigmon et al, 2009)."

What if I were to tell you that caffeine has a negative side effect to your health, would you continue to drink it? Caffeine has been linked to hypertension, increased anxiety, nervousness, irritability and nausea. So why can coffee taste that good but have some many side effects? "These behavioral and physiological effects of caffeine occur primarily through antagonism by caffeine of the action of endogenous adenosine at adenosine A1 and A2A receptors (Fredholm et al, 1999)." This study has linked a SNP between caffeine and increased anxiety. "Specifically, it was found that 150 mg caffeine (equivalent to the amount of caffeine present in, eg, 1½ cups of ground coffee) increased anxiety in individuals carrying the TT genotype of the ADORA2A SNP rs5751876, but not in the CT and CC genotype groups (Alsene et al, 2003; Childs et al, 2008)." This study took 218 women and 198 men and administered two doses of caffeine 100mg in the morning and 150 mg shortly after. There was randomization on who would receive caffeine and who would have a placebo. The group of people took a pre-survey to make sure that all caffeine users drank approximately the same amount of caffeine. The day before the study, subjects were not allowed to drink anything that had caffeine in it. Surveys were given to check the anxiety, alertness and quality of headache.

"Another key finding of this study is that a clear anxiogenic effect of caffeine, larger i individuals with the ADORA2A rs5751876 TT genotype, was observed only for people who habitually consumed little or no caffeine (the N and L groups). Higher caffeine consumption appears to lead to substantial tolerance to this effect." They discovered that people who continue to drink caffeine at a high enough rate didn't experience the increased side-effects. They discovered that the subjects developed a tolerance to the caffeine. "Although frequent caffeine consumers experience minimal increased anxiety after caffeine consumption, they are at risk of at least two clear adverse effects of acute caffeine abstinence, namely low alertness and increased headache."

To sum it up people who are habitual users do not develop adverse side effects until they withdraw from the caffeine use. There is also research that has linked a SNP to increased anxiety secondary to caffeine assumption.
For reading of full article please visit http://www.nature.com/npp/journal/v35/n9/full/npp201071a.html

We Americans are so accustomed to a lifestyle of instant gratification, ease, and leisure; especially when making daily choices of what we consume individually. It's no surprise we face an unprecedented epidemic of obesity in this nation when you look at how corporate food companies cater to our demand for easy availability of virtually any type of food one could ever crave. Obviously location takes an important roll as well, but for most of us residing in urban areas, our communities are saturated with endless food options. We no longer need to get out of our car to get an eight-hundred calorie caramel macchiato in the mornings. There's something to be said about the fact that one can obtain endless high-fat and high-caloric meals at the very thought of hunger.

Researchers and statisticians seem to be very compelled in not only updating the nation's obesity statistics, but also in finding new ways to potentially counteract America's modern obesity outbreak. In the past, some of us have resorted to other behaviors and procedures in compensation such as workout rituals, personal trainers, diet pills, and even extreme actions like stomach-stapling, liposuction, etc. Regardless of whether they worked or not, it's about time something new came around.

In last month's publication of Nature & Neuroscience, and interesting study using mouse mutants to research insulin receptor function in the ventromedial nucleus of the hypothalamus (VMH). Provided that high-fat diets lead to the production of severely high levels of insulin (which we all know can initiate cascades of detrimental health issues such as diabetes, high blood pressure, etc.), Klöckener et al. suggest brain mechanisms in the VHM which if genetically modified, may be applicable to humans and anti-obesity treatments.

The VMH is a rather unclear and grey portion of the brain in terms of the knowledge that we currently know about it. We do know however, that it serves as one of the primary locations in the hypothalamus that mediates nutrient sensing, metabolism, and insulin receptor signaling. To guarantee an optimal energy environment for reproduction, the body monitors energy availability indirectly with the help of insulin and leptin that consistently circulate in the body. These two hormones can act to store fat as well as alert other metabolizing processes.

Steroidogenic factor 1 (SF-1) positive cells distribute across large parts of the VMH are directly involved with controlling systematic metabolism. These cells are highly responsive to insulin. Klöckener et al. identified a subpopulation of insulin-SF-1-positive cells in the VMH distinct from leptin-responsive neurons. They found that the systematic deletion of the insulin receptor in SF-1 expressing cells of the VMH caused no immediate changes in homeostasis. However, when both the control and mutant mice were exposed to high-fat diets, the modified SF-1 cell mice were protected from the development of obesity. It was reasoned that this protection from obesity was due to higher leptin sensitivity, since insulin was rendered useless in the mutant mice. Following this discovery, they found that the reinstatement of PtdInsP3 signaling downstream of the insulin receptor made the mutant mice that were previously protected from obesity, vulnerable again.

Even though all of the processes VMH carries out sill remains unclear, the mechanisms involved with insulin and high-fat diets are becoming clearer. These findings are on their way to future investigations where potential anti-obesity therapeutics may be revealed.

I think it's awesome that researchers are unveiling new methods that can potentially solve this epidemic in the near future and I strongly support such research for the benefit of the population. This compelling issue has not been mitigated to a satisfactory level even with counteracting behaviors as mentioned above. Statistically, just below twenty percent of the population in Colorado is diagnosed as clinically obese. It's ironic thought because Colorado tops the list for the least obese state in the nation. We clearly have to keep working, researching, and making changes in order for a valid solution to be found.

The response of a brain while listening to music is very different than the response of the brain to many other types of stimuli. While observing a scene there is no direct way to see how the brain is processing the image. Many different part of the brain must integrate the cloudy points of stimulation (or lack of stimulations,) pattern recognition, and memory among other things for the person to perceive what it is they are looking at. It is a very subjective experience that is difficult for a neuroscientist to analyze. Sound on the other hand (especially simple rhythmic sound) is often very directly observable by many available neurological measurements including EEGs. This has recently been the center of much attention in neuroscience and had provided fodder for several books including This is Your Brain on Music by Daniel J. Levitin and Musicophelia by Oliver Sacks.
EEG studies of patient response to rhythmic beats is the focus of Tagging the Neuronal Entrainment to Beat and Meter from the Journal of Neuroscience published this July. This study tries to delineate how the human mind processes beats and meter in general. Previously many studies were done exploring how musical meter can create an expectation in the listener, you have probably experienced this yourself by tapping your foot to a song you?ve never heard before. Most music (maybe excluding some jazz and freeform types of music) follows some predictable pattern and our brains zero in on them (wonderful recognizers of pattern that they are.)The theory of resonance has been proposed to explain these observances hypothesizing that after certain exposure to the rhythmic beats (or music) large groups of neurons become ?entrained? and resonate at frequency correlating with the music?s beat. By altering the beats from what is expected scientists have studied what the call evoked potentials (or EPs.)
In the studies done in this particular article researchers at the Institute of Neuroscience of the Universite Catholique de Louvain in Brussels, Belgium had participants listen to a 2.4 Hz beat an imagine it as either a binary beat (1 2, 1 2, 1 2, as in a march) or ternary (1 2 3, 1 2 3, 1 2 3, like in a waltz.) As a control they had some participants listen to the beat but did not instruct them to image a particular meter. They then monitored the response of the participants? EEGs. The researchers found that EEGs showed increases in amplitude of subharmonic frequencies in the groups that were imagining the binary and ternary beats. That means in the control group they showed a strong 2.4 Hz signal the binary group showed strong 2.4 and 1.2 Hz signal and the ternary group showed strong 2.4, 1.6, and .8 Hz signals. This supports many of the previous research done on this topic showing that direct observation of the physical experience of music can be measured and quantified using existing mode of neurological research. This may open doors to understanding how the brain processes other types of stimuli and art in the future.

Depression... Baby or no Baby?
"Postpartum depression (PPD) affects up to 19% of all mothers and adversely influences maternal adaptation to motherhood (Gavin et al, 2005) with negative effects on child development, as children of depressive mothers are more vulnerable to develop mental disorders in later life." (Grace et al, 2003)

Every father remembers the day they found out that their wife was going to have a baby! With all the excitement, most fail to acknowledge the mood swings between trimesters and well after the pregnancy. There is more to pregnancy then peanut butter and pickle sandwiches. So, what gives? As the growing baby starts to develop so do new hormones and hormone levels also increase.

Oxytocin is one of the first identified polypeptide hormone also known as the "love hormone." Oxytocin is responsible for increase bonding feeling associated with pregnancy. This study suggests that low levels of oxytocin have a higher risk of postpartum depression. There are other risk factors that can increase chances of postpartum depression such as age under 20, drug/alcohol abuse, increase emotional vulnerability and lack of support.

This study proposed by National Centre of Competence in Research (NCCR) Swiss Etiological Study of Adjustment and Mental Health took 75 pregnant females and tested their levels of oxytocin during the last two weeks of their third trimester along with two weeks after giving birth. After their study they concluded that increasing the level of oxytocin during pregnancy could decrease the severity of postpartum depression.

The researchers did their best to find equal candidates for the study. The research was focused on same age females within the same economic status along with a healthy pregnancy. "A detailed study description was given to all interested women and, if any raised, questions were answered. All participants were screened for the following inclusion criteria: (a) no current mental illness, (b) no severe medical complications (acute or chronic physical diseases, such as gestational diabetes, metabolic diseases, hypertension and thyroid dysfunction), (c) no signs of fetal malformation, (d) a pre-pregnancy BMI below 32, (e) no smoking beyond the 10th week of gestation and (f) good knowledge of German language."

The researchers also discuss that this is one of the first studies done to link postpartum depression and oxytocin levels. They stated that more research needs to be done to see if increasing the levels of oxytocin could help prevent postpartum depression in females. One thing that they acknowledge is that the environment could be influencing the sign and symptoms of postpartum depression.

This was very informational article about oxytocin and postpartum depression. One thing that I find myself amazed on is that oxytocin is also given to induce labor. If increasing the levels helps prevent postpartum depression at what point do we higher the levels, hours before pregnancy, days before or weeks before? If we raise the level, will this also induce labor at a unsafe time in pregnancy?

If you are interested in the original article please reference this online journal at http://www.nature.com/npp/journal/v36/n9/full/npp201174a.html

In Mike Nichols film "The Birdcage," Albert played by Nathan Lane, is an insecure, emotional-rollercoaster drag queen whose partner Armand, played by Robin Williams, is an unwavering, cautious entrepreneur. Albert's insecurities get the best of him on stage in addition to his relationship woes that cause him to act in a neurotically unstable fashion. When his self-image gets the best of him, he relies on "Pirin" tablets supplied by his houseboy to calm his nerves and give him so called confidence so he can perform on the stage, and keep the guests coming. Completely clueless to the fact that the "Pirin" tablets are just aspirin tablets with the "A" and "S" scratched off, Albert's "need" for them remains a religious habit.

Albert's surrender to the placebo effect isn't necessarily out of the norm when taking the general population into perspective. Research published in the Journal of Neuroscience surrounding the neurobiological mechanisms of the placebo effect could be used as an excuse as to why people like Albert succumb to pseudo-western medicine prescriptions and expectations to better their condition.

The placebo effect is a psychobiological phenomenon that can be attributable to different mechanisms, including expectation of clinical improvement. In Fabrizio Benedetti's research encompassing this effect, he notes that no matter what medical treatment a patient is receiving, their therapeutic outcome is surrounded by psychosocial contexts. The placebo effect has become a modern topic of interest among scientists and the general public in light of the fact that "we must broaden our conception of the limits of endogenous human capability."

If we can rely on our own homeostatic processes and reduce our usage of unnecessary western medications, some of which have detrimental side effects later in life, we can potentially better our overall well being. In Parkinson's disease research, a pool of patients was given an inert substance (the placebo) and were told that it was an "antiparkinsonian drug that produces an improvement in their motor performance." Results displayed that with their capability to measure endogenous dopamine release, the placebo-induced expectation of motor improvement activates endogenous dopamine in those patients. This ultimately led the patients to better therapeutic outcomes.

We know that the placebo effect is real. Patients involved in thousands of placebo-induced studies have shown a better therapeutic outcome when their expectations and knowledge of recovery is good. Recent uproars are now suggesting the idea of anti-depressant medications being glorified placebos. On account of the pharmaceutical boom for mental illnesses, scientists are heavily researching not only the accuracy of such drugs but the validity.

What does this mean for the Albert's of the world and the rest of us taking conceptually risky medications? Well, even though the thought of people halting their prescription use and relying on their endogenous human capability to run the ship seems amiable, it's not practical. People need medications. However, I definitely think pharmaceutical companies are where the problem lies. How do we know that the neurological drugs that our doctors are telling us we need are in fact necessary or even beneficial for that matter? We don?t. But there's no reason why we shouldn't question the men and women who attended a higher level of education to write us these prescriptions.

Those of us in dating in high school in the late 80′s can attest to the stinging truth revealed in Def Leppard?s song, ?Love Bites? shortly after a nasty break-up. But it was only recently that scientists employing state-of-the-art brain imaging fMRI technology have been able to view the similarities between the biting pain of rejection from a lover and physical pain.

A study published in the April 12 issue of Proceedings of the National Academy of Science (PNAS) has provided the most direct evidence showing a common brain circuit underlying the pain of rejection and physical pain.

In their study, the researchers at Columbia University, University of Michigan and University of Colorado, Boulder studied 40 subjects who had experienced rejection and break-up with a lover within the past six months. They tested each subject on two tasks, a social rejection task and a physical pain task, while imaging their brains.

In the scanner, subjects looked at the faces of their ex and thought about how it felt during their split and a snapshot of their brain was taken. Next they were shown a headshot of a friend of the same sex as their former partner and thought about a recent positive experience they shared. This provided the social rejection condition.

To compare the social rejection experience to the experience of ?physical pain? they attached a thermal device to the volunteers? forearms and set it to produced a ?painful?, but not harmful level.

In both men and women, rejection and painful heat activated brain circuits underlying distress (e.g. Anterior Cingulate cortex) and the sensation of pain e.g. somatosensory cortex).

Although this seems seems intuitive from centuries of poetry, tragic plays and lyrics, knowledge at a mechanistic level showing the same circuits are activated gives scientists new ways to deal with both. It makes one wonder if taking pain-killers shortly after a break-up might be a treatment option.

The common mechanism between social rejection and physical pain may be one reason why heroin and alcohol, both analgesics for pain, are irresistible amongst country and grunge musicians whose melodic ruminations center on tragedy, angst and painful relationships. Kurt Cobain comes to mind when he said, ?Thank you for the tragedy. I need it for my art.?

Last year the British pop group ironically named, ?The Wanted?, brilliantly connected the idea that pain from being unwanted/rejected and searing physical pain were one and the same in their popular song ?Lose My Mind?. Here are the lyrics and the video

They say that time
Heals everything
But they don?t know you
And the scars you bring

?Cos you left a jagged hole
And I can?t stand it anymore

If heartache was a physical pain
I could face it I could face it
But you?re hurting me
From inside of my head
I can?t take it I can?t take it

I?m gonna lose my mind
I?m gonna lose my mind

I?d erase my thoughts
If only I knew how
Fill my head with white noise
If it would drown you out
Kill the sound

If heartache was a physical pain
I could face it I could face it

But you?re hurting me
From inside of my head
I can?t take it I can?t take it

I?m gonna lose my mind
I?m gonna lose my mind

And I?d rather be crazy
I?d rather go insane
Than having you stalk
My every thought
Then having you here inside my heart

If heartache was a physical pain
I could face it I could face it
But you?re hurting me
From inside of my head
I can?t take it I can?t take it

I?m gonna lose my mind
I?m gonna lose my mind