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December 3, 2011

Drinking on the Job: How Flies get Drunk


Thursday, Friday, and Saturday night... I know what you're thinking. No class till Monday, no work, what a great night to get ahead on studying and up to date with all the problems in the world. However, I must point out this plan is not the first thing that pops into everyone else's mind (at least those outside the world of the poor soul who is reading this neuroscience blog). Much of western society is based around the beverage/drug/poison we've come to know as alcohol. It has come to the attention of neuroscientist that our race is not the only one that takes pleasure in consuming firewater. It turns out some researchers were playing with the old 160 proof lab ethanol when they came upon an astounding discovery.

It all started when one turned to the other and croaked, "I'm drunkk frog haha." The other slurred back, "weelll thenn, gooood thing I'm not a fly huh?" That's when it hit them. "Eureka!" piped the first. "Oh my god!" yelled the second. "Let's" get the flies wasted!" the second hollered back. They quickly spun off their lab stools and bustled for the fly room stumbling and tripping the whole way. When they got to the room they immediately grabbed the first beaker of flies, ripped out the cork and filled it full of the powerful booze, instantly killing all the flies inside. Once they realized the horrendous massacre they had just committed in front of all the hundreds of thousands of other flies in the room their drunken smiles slipped off. The beaker was placed on the counter as the two somber scientists held each other with silent tears streaming down their cheeks. Then one started laughing; irritated, the other muttered, "How can you laugh at a time like this? We just killed them, in front of their families... drowned them, squashed them like flies... "Look, that one's drunk," the other researcher pointed at a fly that was clearly not adhering to the standard sober drosophila flight pattern. They watched the fly for nearly two hours, they sat on the fly room floor entranced by the fly's drunken escapades. Then as its flight pattern began to return to normal it headed back to the beaker full of booze, and began gulping down, without a thought to the dead brothers, sisters, cousins and children floating on top. Gleeful laughter burst from the researchers as they cheersed and began taking large quaffs of their own. Quickly forgetting their bloody hands they then began pulling the corks of the other beakers, filling up petri dishes with ethanol, and pipetting small volumes of ethanol in for the larvae--so no one was left out. They spent the whole night at the lab with their new found drinking buddies and had a gay old time. A few days later after their handover was gone they decided to write a paper.

It was determined drosophila liked the inebriation caused by excessive consumption of ethanol. Like us, the flies were experiencing their pleasure through the activation of the dopamine pathway. Activating this pathway induced LTP in the flies. Looking further into the flies' neural circuitry the researchers determined the rewarding memories the flies experienced (or the lack of memory if they got too plastered from not getting enough sugar before) were localized, accessed and retrieved with a distinct set of neurons in the mushroom body. With the vast number of flies they got drunk the researchers' found some flies didn't come back to drink. The experimenters were obviously offended and quickly squashed them. However, they didn't stop there; they proceeded to analyze the DNA so they could breed out the bad gene and make sure no other flies would be lame. They found mutations in scabrous were responsible. They commonly call it the party pooper gene around the lab. "This gene encodes a fibrinogen-related peptide that regulates Notch signaling, disrupted the formation of memories for ethanol reward" (Kaun, 2011). The experimenters have been thought to have had a little bit too much fun drinking with the flies, but they have felt the public pressure. Now they're looking into how this research will help their own species and we will undoubtedly be hearing more from them soon.

Hope you enjoyed the read, sincerely Charlie Stewart

"A Drosophila model for alcohol reward"
Karla R Kaun, Reza Azanchi, Zaw Maung, Jay Hirsh & Ulrike Heberlein
Nature Neuroscience April 17th 2011
Posted by      Charlie S. at 8:15 PM MST
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December 2, 2011

Alcoholism: Can it be Cured?


Alcoholism to this day is one of the most deadly and chronic diseases, that is interestingly controversial with regards to symptoms, treatment, diagnosis, and even heritability. How can a disease be so dangerous and historical and yet not even be remotely understood? As medicine, science, and technology move forward we are rapidly moving towards this inconceivable goal, but treatment is still only moderately successful along with progressive pharmacotherapies for all addictions.

A huge part of this lack of understanding of this disease is the fact that alcoholics are all different in a variety of ways; including their symptoms. There are numerous biological mechanisms as a result of alcohol addiction, all of them varying in their manners and withdraw. So recent studies show that these different mechanisms represent different stages of alcoholism, which could be relieved by different treatments. Regardless, these treatments have to block motivation to seek and consume alcohol.

Researchers have determined two categories: relief and reward drinkers. Reward drinkers drink to reward themselves the same way many drugs work, by activating brain reward pathways. Relief drinkers drink to relieve negative emotions, such as anxiety and feelings of withdrawal. Obviously these two varying types of alcoholics require different treatments.

It has also been discovered that alcoholism is marginally heritable. Genetic susceptibility is an alcoholic trait that can be passed down from generation to generation, however these varying types of alcoholism are largely based on environmental factors. These would include things such as how often the individual is exposed to stress or put in a circumstance of reward.

So now, is it possible to treat either one or both of these forms of alcoholism? Studies show that the reward system of alcoholism is mediated by a collaboration of endogenous opioids and dopamine release. Activation of dopamine in the mesolimbic pathway has been correlated to many other sorts of drug addictions. Dopamine is regulated in the corticomesolimbic system by a receptor known as MOR (mu-opioid receptor), which if blocked, prevents dopamine release caused by alcohol consumption. A drug known as naltrexone is an antagonist of opioid receptors, and is currently being researched as treatment for reward alcoholics.

Next is relief drinking. Relief drinkers drink to suppress stress, anxiety, discomfort, pain, and dysphoria. These alcoholics generally end up setting the stage for routine and frequent alcohol consumption to escape negative emotions. Recently, it has been discovered that release of CRF is central to this behavior. CRF (Corticotropin-releasing factor) is a peptide that is released into the anterior pituitary by alcohol consumption in relief drinkers, which in turn releases ACTH and stimulates cortisol release, reducing stress. CRF regulation and function is somewhat genetically determined, which makes a pharmacological cure more difficult and less likely to be successful. However, studies have shown that in individuals with naturally decent regulation of CRF could likely be treated for relief alcoholism; via CRF1 antagonism. Research is still ongoing as to whether this would be a sufficient method to treat alcoholics.

Alcoholism is a very complex disease, by which human understanding is challenged and pushed to therapeutic limits. This blog marks a tremendous step in the right direction towards understanding alcoholism and possibly curing the disease one day, but until that day comes there is plenty more to learn and to gain.

Heilig, Markus, David Goldman, Wade Berrettini, and Charles P. O'Brien. "Pharmacogenetic Approaches to the Treatment of Alcohol Addiction : Article : Nature Reviews Neuroscience." Nature Publishing Group : Science Journals, Jobs, and Information. 20 Oct. 2011. Web. 02 Dec. 2011. .

http://www.nature.com/nrn/journal/v12/n11/full/nrn3110.html
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October 23, 2011

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.
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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...

Source: http://www.nature.com/neuro/journal/vaop/ncurrent/full/nn.2934.html
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