NRSC 4132 Blog

It is difficult to find someone who truly has not seen the atrocious affects of drugs on a person. Whether it be a close friend or family member, an ad in a newspaper, or one of those haunting Colorado-Meth-Project commercials, the word is out: drugs kill. And they are killing more and more than ever before.

The dangers of addiction are widely known, yet countless lives are constantly being enslaved to the heinous power of addictive drugs. Thus, addiction is the area of interest in countless labs across the world. Understanding the neurological pathways of drug addiction is vital in the ongoing "war on drugs" that seems like it will never come to a halt. In fact, according to the Mayo Clinic, 19.5 million people over the age of 12 use illegal drugs in the United States [1]. But, if there is a chance of recovery and relief, it is my belief that it will not come from lawmakers or the police force, but rather from the realm of science.

One such study was published in Neuron this year: Potential Vulnerabilities of Neuronal Reward, Risk, and Decision Mechanisms to Addictive Drugs. It sought out to explore how the normal, physiological reward processes can be affected by addictive drugs. It all came down to changes in acute responses and plasticity in the brain, specifically dopamine neurons and postsynaptic structures. Dopamine has many functions in the brain, including important roles in behavior and cognition, voluntary movement, motivation and reward, inhibition of prolactin production (involved in lactation), sleep, mood, attention, and learning [2].

These effects reduce reward discrimination, increase the effects of reward prediction error signals, and enhance neuronal responses to reward-predicting stimuli, which may contribute to compulsion [3]. Addictive drugs increase neuronal temporal reward discounting and generate temporal myopia, which impairs the control of drug taking.
The experiment also found that long-term enhanced dopamine levels may disturb working memory mechanisms necessary for assessing background rewards. Thus, drugs may generate inaccurate neuronal reward predictions. Drug-induced working memory deficits may also impair neuronal risk signaling, promote risky behaviors, and facilitate preaddictive drug use. Malfunctioning adaptive reward coding may lead to overvaluation of drug rewards. Many of these malfunctions may result in inadequate neuronal decision mechanisms and lead to choices biased toward drug rewards [3].

Studies like this are incredibly important not only to drug-users and their loved ones, but to society as a whole. I will never forget the day I met a homeless man in Denver who asked me if you can fly on a plane if you have a warrant out for your arrest. I learned that he was trying to get home to his family in Michigan after ten years of being away. One day at work he was feeling really low and tried some "white powder" and he saidwithin a few months he lost his job, his family, his friends, his home... But the one thing he still had the day I met him was hope, which is inspiring to all, for society can only move forward as a united front that has overcome the trials of addiction.

[1] http://www.usnodrugs.com/drug-addiction-statistics.htm
[2] http://www.news-medical.net/health/Dopamine-Functions.aspx
[3] http://www.cell.com/neuron/abstract/S0896-6273%2811%2900112-7

The age old question of size has finally been answered and it turns out it does matter. If you want to be popular then being big is best, but not in the way you think. New England researchers reported in the prestigious journal Nature Neuroscience (December 26, 2010) that human amygdala size correlates with the extent and complexity of one's social life.

Using a technique from Harvard called FreeSurfer which reconstructs brain images from structural MRI scans and has the capability to overlay fMRI data, the researchers measured the sizes of multiple brain structures and cortical thicknesses of 58 adult men and women. Then they questioned the participants about their social lives, looking to find out how many regular contacts they had and also looking at how complex their social lives were, using the number of distinct social networks within the whole social life as a measure. Participants had anywhere from 4 to 50 contacts and 1 to 7 distinct networks.

They found that the amygdalas of the participants varied in size considerably with the largest being over twice the volume of the smallest. The regression coefficients they found were pretty solid at 0.38 for the relation between the number of contacts and amygdala size and 0.44 for the relation between number of networks and amygdala size. They also measured a bunch of other brain structures to check for correlations but didn't find any except for some slight matches between cortical thickness in three areas that would be expected to contribute to social competency, the anterior cingulate gyrus, for instance.

How exactly that relationship comes about is a topic for discussion. The amygdala is usually thought of as the fear center of the brain so seeing that it's correlated with a larger social network is a somewhat surprising result. Does a larger amygdala make it easier to suppress fear and so people feel less anxiety in social situations, leading to a more active social life, or is the largeness of the amygdala an indicator that a person is generally more fearful and so cleaves to their social life in an effort to buffer themselves from the fearsome natural world? The researchers believe that the larger amygdala helps people distinguish between welcoming and threatening social situations, thus leading to greater social competency and greater social capacity.

It's also possible that the amygdala has more than one distinct function. Maybe it's not just the subcortical structure that makes people feel fear but can also process social data. It would be terribly interesting to find a way to turn the activity of the amygdala down and then measure people on their ability to understand social cues or their accuracy when trying to determine whether certain social situations are dangerous or not. The connection is really very exciting and opens up a whole new area of research opportunities.

Most important of all is what it could mean for everyday life. Understanding the mechanisms that link the amygdala size to social success could highlight a set of social skills that would help people enhance their social lives. Maybe people who aren't as socially successful could improve their social lives just by paying closer attention to whether social situations present a risk, for instance.

This is exciting news that helps make steps toward simplifying the great mystery of social living, this one as simple as knowing where the danger lies as a key to success.

Have you ever spoken to someone who was just a little "off" and wondered if their brain was wired differently than yours? What about yourself, have you ever speculated that your own brain may have missed a few connections? While there may be some differences between how your brain functions compared to some average joe down the street, it's likely that these differences are not significant. In general most neurotypical people have similar connections between the different brain regions. One group of atypicals, however, has shown disparities in the active connections when performing various tasks. This group is composed of those with Schizophrenic symptoms.
While there have been a few studies conducted concerning the functional connections in select brain regions for Schizophrenics, there has been little conclusive evidence due to their specific nature. One study by Solomon et al. 2011, attempted to encompass all of this information by analyzing the entire brain while having groups of people perform several cognitive tests and also resting. To confirm which brain regions were activated, each subject underwent functional magnetic resonance imaging while performing these tasks. The cognitive tests performed by the subjects included n-back memory tasks along with a verb generation task. During the n-back memory task, the participants were asked to identify when an image matched one they had seen in a sequence n-number of images before. This is very similar if not identical to some training sessions in popular phone apps designed to improve cognitive function such as Memory Trainer. In the verb generation tasks, the participants were given a series of nouns and must think of a verb that corresponds with it. All participants were a mixture of male and female right handed individuals between the ages of 19 and 39 years old. Of the group of schizophrenic participants involved in cognitive testing, all were patients at the Tirat Hacarmel Mental Health Center. Each of these patients had been medicated with either haloperidol or an atypical antipsychotic drug and had been for an extended period of time.

Despite the fact that both the control and experimental (schizophrenic) groups were performing the same tasks, there were disparities between the overall brain regions excited by these tests. The brain images from the schizophrenic group were averaged along with those from the control group and compared. The resulting data shows disparities between the various groups for each task. The main regions of disparity during the n-back task were the superior frontal gyrus, central sulcus precuneus, inferior parietal lobe, inferior temporal gyrus and the fusiform gyrus. The disparity between neurotpicals and schizophrenics was even higher for the verb generation tasks and included the regions of the premotor cortex, post central sulcus and gyrus, intraparietal sulcus and the anterior cingulate gyrus. Not only does Solomon et al. show that there may be different connections in the brains of those with chronic schizophrenic episodes but they are many and varied.

Solomon et al. proves that not only is it possible to have your brain wired differently, but that it happens in real life with groups of those with atypical neuronal and psychological activity. Perhaps the next time you feel someone is a little off, remember that there is a strong possibility that their brain just uses different connections than yours.

Source:
Salomon, R., Bleich-Cohen, M., Hahamy-Dubossarsky, A., Dinstien, I., Weizman, R., Poyurovsky, M., . . . Malach, R. (2011). Global functional connectivity deficits in schizophrenia depend on behavioral state. Journal of Neuroscience, 31(36), 12972-12981. doi:10.1523/JNEUROSCI.2987-11.2011

In the early ages, mankind was very segregated. There were nomads, warriors, hunters, etc. who occupied distinct geographical areas and practiced a very specific way of life. Over time, these cultures began to mesh, and today, nearly every nation is comprised of constituents hailing from all parts of the globe.

Interestingly, a recent study in Nature Neuroscience (http://www.nature.com/neuro/journal/v6/n12/abs/nn1156.html) indicates a neural mechanism for the integration of cultures. Specifically, Jennifer Richeson et. al conducted fMRI studies that identified regions of the brain allocated to repressing racial biases and prejudices.

Jennifer Richeson et. al designed their study to examine a previously proposed theory called "resource depletion". Prior research suggests that central executive processes are recruited "to combat the expression of stereotypes and negative attitudes that often come to mind automatically and unintentionally". The resource depletion theory postulates that the suppression of racial attitudes upon interracial contact temporarily depletes central executive control, and hence, performance on tasks requiring central executive control following interracial contact is diminished.

The study consisted of two experiments conducted on 15 Caucasian, American undergraduates. The first experiment involved individuals completing a survey on racial bias, then interacting with a black individual, and then completing an unrelated Stroop-color naming test that assesses executive control. In the second experiment, these individuals were presented with pictures of unfamiliar male black faces, and fMRI imaging was used to examine the activity of brain regions implicated in executive control during and immediately after the images were presented.

The fMRI imaging revealed heightened activity in the dorsolateral prefrontrol cortex (DLPFC) in individuals that exhibited racial biases. As expected, this increased activity in the DLPFC correlated to diminished performance on the Stroop-color naming test, indicating that executive control resources had been depleted following interracial contact. In contrast, there was no heightened activity in the DLPFC in controls (those who did not show racial biases on the initial survey), and these controls did not show diminished performance on the Stroop-color test.

The DLPFC is believed to directly influence the engagement of inhibition responses, such as suppression of racial biases. Another area of interest, the anterior cingulated cortex (ACC), is believed to sense situations/circumstances when such control is necessary. While fMRI imaging revealed increased activity of the DLPFC and ACC in racially biased individuals, only DLPFC activity correlated to diminished Stroop-color test performance. This indicates that while both areas may be important in regulating racial biases, the DLPFC region more directly affects performance on executive control tasks following interracial contact.

It is surprising that regions of the brain function to repress racial biases and stereotypes. More research is needed to identify what brain structures contribute to the development of these biases in the first place. Perhaps such research will lead to the development of drugs that promote cultural awareness and tolerance, something we could all use a dose of.

We all may like to think we perform random acts of kindness all the time, like watching someone's laptop at the coffee shop while they step out to take a phone call. But you cannot deny that you consider how you will benefit from many of the decisions you make. Well, you are not alone, and now scientists know why. But first, in order to truly grasp the significance of this study, take a second to consider what the word "guilt" means to you. When was the last time you felt guilty? Can random strangers evoke this feeling inside you, or do your loved ones hold all the power?

Whether it is cutting someone off on the highway or having an affair that ruins a marriage or anything in between, guilt is usually a feeling we try to avoid. The article Triangulating the Neural, Psychological, and Economic Bases of Guilt Aversion defines guilt as "a negative emotional state associated with the violation of a personal moral rule or a social standard and is particularly salient when one believes they have inflicted harm, loss, or distress on a relationship partner, for example when one fails to live up to the expectations of others." Thus, the decision to watch over the laptop might not be economically rewarding, but an attempt to minimize guilt is indeed in one's best interest. This idea suggests that people do care about the payoffs of others and ultimately, a greater state of social cooperation is achieved.

A truly fascinating study utilized a formal model of this process in conjunction with fMRI, a noninvasive test that uses a strong magnetic field and radio waves to create detailed images, in this case of blood flow in the brain to detect areas of activity. The study successfully identified brain regions that mediate cooperative behavior while participants decided whether or not to honor a partner's trust. It found that "a neural system previously implicated in expectation processing plays a critical role in assessing moral sentiments that in turn can sustain human cooperation in the face of temptation." So what is the point here?

The fact that different areas of the brain were activated when participants chose to abuse trust to maximize economic self-reward rather than avoid guilt shows the importance of expectations in one's decision making. So next time someone asks you to keep an eye on their stuff, know that your insula, supplementary motor area, dorsolateral prefrontal cortex, and temporal parietal junction are hard at work, preventing you from feeling that pit in your stomach when the guilt creeps in.

Certainly, this breakthrough study has graced our knowledge with precious clues into the mechanisms that underlie the behaviors of trust and reciprocity. By understanding the neural circuits that underlie cooperative behavior, we are one step closer to a safe and successful society.



Resources:
Article from Neuron:
http://download.cell.com/neuron/pdf/PIIS0896627311002996.pdf?intermediate=true
How Stuff Works:
http://science.howstuffworks.com/fmri.htm

Focus on your breathing. As thoughts and emotions come to you, simply observe without judgment and dismiss them, as if they were just passing by outside your car window. Return to the sensations of air passing in through your nostrils, down your trachea and filling your lungs...

Sound like a yoga class? Hypnosis? Close, but even better. It's a trick you can keep up your sleeve to pull out the next time your body screams "Ouch!" And it works, according to a study published in the April, 2011 issue of the Journal of Neuroscience. (https://cuvpn.colorado.edu/content/31/14/,DanaInfo=www.jneurosci.org+5540.full.pdf+html)

Researchers took 15 young healthy volunteers, and applied a painful stimulus to their calves for about 6 minutes while instructing them to simply pay "attention to breath." Brain activity was recorded using fMRI before and during the noxious stimulus. Afterwards, the subjects also rated their subjective pain intensity and pain unpleasantness on a standard visual analog scale.

Subjects were then given instruction in Shamatha, a type of "mindfulness meditation" that involves focused attention on the sensations of the breath, while disengaging from intrusive thoughts or emotions. Subjects spent merely 20 minutes a day, for 4 days, learning the technique. The fMRI sequences were then repeated, with the subjects meditating as taught during the application of noxious stimulus.

Meditation has long been thought to modify our sensory experiences, but the specific brain mechanisms were mysterious. As expected by the researchers, the subjects' ratings of pain intensity and pain unpleasantness were lower during meditation than before the training. In fact, subjects rated their pain lower by 40% and 57% respectively!

New information also emerged. Several different brain mechanisms seemed to be working at once. fMRI showed that distinct brain regions were significantly more active during meditation, some of them associated with the cognitive modulation of pain; some related to emotion regulation; some tasked with reframing the contextual evaluation of sensory events; and others involved in interoceptive awareness (attention to sensations inside the body). Additionally, some areas such as the thalamus were deactivated during meditation, acting as a sort of gatekeeper for afferent nociceptive signals.

Thanks to these brain mechanisms, you can handle the pain - if you make friends with Shamatha. For a relatively small time investment (just 20 minutes a day for 4 days), you can acquire a skill that will last you a lifetime, and hone it with practice. By extension, the pain-reducing benefits of Shamatha could be used to brave a variety of "painful" circumstances, like speaking in front of a crowd or meeting your boyfriend's parents. Further, a host of other benefits of increased interoceptive awareness await, like "trusting your gut" or knowing when you need some exercise, or knowing when you've had enough pizza.

Try it; it can't hurt.

Syntax and grammar, the fundamental rules of any language can make many school aged children emit a resounding "Ugh!" These are strict rules that we have developed over time to help keep our evolving languages in check: they tell us what order to put words in and what words are to go together. It is even possible to use the rules our own language to decipher other languages. We do this by first assessing the grammar, because humans have the ability to determine grammar despite a lack of context. This would have been essential for anyone attempting to learn a new language for the first time: recognize the patterns and go from there. For instance: in English, the verb tends to be in second position within a sentence but it can be almost anywhere; in German the verb is only in the first, second and last position within a sentence. This too can be used to study dead languages such as Mayan, which has been found to place the verb first in the sentence.
The ability to discern these patterns resides in Broca's area, or the left inferior frontal gyrus within the human brain. Studies on the analogous structures in nonhuman primates have only shown an ability to process simple sequences, failing at understanding complex language structures. It has since been thought that the comprehension of intricate communication was reserved for our own species.
One study, "Songbirds possess the spontaneous ability to discriminate syntactic rules," by Kentaro Abe and Dai Watanabe debunk this previous assumption. To show that songbirds can indeed asses the 'correctness' of a song, a mixture of both store bought Bengalese finches and those that were raised in an aviary were placed in a room with a speaker. This speaker was to play songs that the bird had been habituated to (such as those it would have learned from others of its species as it matured), along with new songs and the original with modifications to the sequence of notes. The determination of whether these sequences were discriminated against was the amount of vocalizations, with a higher number indicating a discrepancy in syntax. In both male and female finches, there was a significant increase of bird calls when specific sequences were changed against the rules of their syntax, while others did not elicit a response. This suggests that not only are certain songbirds able to listen to auditory information and glean syntactic rules but are also able to use this information when examining novel auditory information.
The faculties needed to decipher syntax seems to be a learned response, however. In birds that had been isolated from the general populous excepting for their nest mates, their ability to discriminate non-syntactically correct sequences was significantly lowered compared to controls. This was enhanced as they approached maturity, but did not improve any further while still in isolation. When these isolated birds were then moved to an aviary, they learned to distinguish correct and incorrect syntax as determined by their peers within two weeks, a blink of an eye compared to the amount of time that humans spend on learning our own syntax.
This ability shown by finches and other song birds is a complex system of communication and just may show that humans are not alone in their capacity to communicate.

Original article found at: www.nature.com/neuro/journal/v14/n8/full/nn.2869.html
-edited for punctuation-

As children, many of us had the elaborate dream of becoming professional athletes. We saw their glorified images painted on buildings and billboards, constantly highlighted on TV, and passionately reviewed on the front of each week's newspaper. The professional athlete was - and still is - a symbol of unprecedented talent, glory, and fame, the highest of all achievements.

Unfortunately, that dream goes unrealized for the vast majority. As the New York Times reports, the chances of becoming a professional athlete is 24,550 to 1, "so you have a better chance of getting struck by lightning, marrying a millionaire, or writing a New York Times bestseller."

But what makes becoming a professional athlete so difficult? Recent scientific research has unraveled part of the problem, reporting that the average athlete spends approximately 10,000 hours of deliberate and focused practice. To put this into perspective, imagine spending 2 hours every day practicing; at this rate, it would take 14 years of non-stop practice to reach the level of a professional.

While this task seems near impossible for the majority of us, a nascent field of neurological research is emerging that may hold the key. With the advent of novel technologies such as fMRI (first discovered in the 1990's) and transcranial magnetic stimulation (TMS, FDA approved in 2008), neuroscientists have been able to examine the neural circuitry of professional athlete's to understand what sets them apart on the cellular and molecular scales.

Of particular interest is a paper (http://www.nature.com/neuro/journal/v11/n9/abs/nn.2182.html) published in Nature Neuroscience by Salvadore Aglioti et. al, which examined the dynamics of action anticipation in elite basketball players. Specifically, elite athletes, elite coaches (who hadn't played the sport in several years), and novices (with marginal knowledge of the sport) were presented with videos of basketball players shooting free-throws at time frames varying in duration from 426 - 1,623 milliseconds, and asked to predict whether the shot was good or off target.

As expected, the elite basketball players exhibited the greatest accuracy for the full-length videos. Elite coaches performed comparably, though at a slightly lower accuracy, while novices performed poorly. But interestingly, only the elite basketball players were able to accurately predict free-throw fate for video timeframes before the ball had left the player's hand. This suggests that elite basketball players were able to recognize body kinematics (hand positioning, body posture, etc.) to anticipate the effect prior to ball release.

Previous neuroimaging studies conducted on dancers have identified heighted neural activity in the premotor and parietal cortices during performance of a dance routine. Similarly, tasks involving linking visual familiarity with motor control (such as viewing videos of dancers and identifying when they would make mistakes) resulted in activation of these areas.

Given this precedent, Salvadore Aglioti et. al conducted TMS on the corticospinal system , the principal motor system that innervates the aforementioned areas of the brain. It was discovered that maximal excitability in elite athletes occurred at the 781 ms clip, just before the ball left the player's hand, while it occurred much later for both elite coaches and novices. This suggests that elite athletes posses "extremely fine-grained perceptual operations, like early catching of erroneous or ineffective body configurations". Moreover, only elite athletes demonstrated corticospinal excitability during prediction of missed shots, while the other two groups demonstrated excitability only when predicting made shots.

This results show that elite players are finely tuned to anticipate motor-control errors. While coaches are apt at identifying good shots and correct form, elite players are further versed in anticipating wrong moves by their opponents. Mechanistically, it is proposed that this ability arises from the extensive practice that elite athletes undergo, which strengthens visual-motor synapses in the corticospinal system. As these synapses are strengthened, it takes less of a motor or visual cue to activate neurons implicated in the elite athlete's action anticipation.

If neuroscientists continue to investigate the synapses implicated in elite athletic performance, it may be possible one day to administer agonists that activate untapped reserves of athletic ability. But how ethical is "gene doping"; will it be viewed positively for its potential to elevate the quality of sports, or will it be viewed as a cheap way to avoid 10,000 hours of practice? Only time will tell.

Antidepressants are a part of everybodyâ??s life. Whether its watching multiple brands flash across the TV screen, or you personally take them, the development of effective and quick antidepressants has been the mission of many drug manufacturers in an effort to help the 17% of the population with mood disorders finally get some relief.
People with depression that choose to use medication as treatment are forced to choose between a group of relatively ineffective drugs with adverse side effects including weight gain, constipation, tremors, and many more. In the article â??Silver Bullet for The treatment for Depression?â?? (http://www.sciencedirect.com/science/article/pii/S089662730700623X) by Ronald S. Duman, a study of the 5-HT4 receptor and depression is reviewed an analyzed for the possibility of a faster acting treatment with less side effects.
According to the article, the 5-HT reuptake inhibitors, also known as SSRIs, are the most commonly prescribed class of antidepressant on the market. Although SSRIs initially react within hours or days of a person starting the treatment, due to speculated adaptations in the pre-and post-synaptic clefts; it can take weeks or months for SSRIs to reach their full potential. According to Duman, the reason it takes so long for the drug to reach its full potential is because the treatment must first overcome the desensitization of the inhibitory 5-HT1A autoreceptor. After several weeks of treatment the 5-HT neurotransmitter will continuously fire and release.
The first initial idea came from a previous study that demonstrated that the 5-HT4 receptor agonist reached its maximal effect within three days. This means that the drug can rapidly overcome desensitization of the 5-HT1A autoreceptor. This discovery lead to a more in-depth look at the 5-HT4 receptor agonist with the hope that it could be the quick fix to depression.
Within the deeper research the 5-HT4 receptor agonist was found to have â??a rapid and robust response,â?? (Duman). Not only can this drug mimic the effects of the common SSRIs, it could do it in three days versus several weeks and magnitude was twice as strong in comparison. Beyond just the strong and rapid antidepressant response, the 5-HT4 receptor agonist quickly increases the neurogenesis in the hippocampus. While this is by no means more effective than the antidepressant effects in SSRIs, neurogenesis along with an antidepressant effect can yield to more responsive effects in less time. Also, the 5-HT4 receptor agonists can produce rapid firing and releasing for several weeks without desensitization, which is not common with other antidepressant medications.
Although these mechanism adjustments will yield faster and more successful treatment, a question for anyone starting any medication is in regard to the side effects of the medication. With SSRIs there are many adverse side effects such as: nausea, insomnia, anxiety, weight gain, tremors, sweating, sleepiness, dry mouth, and headaches. Some of these will be persistent, while others will go away within a few weeks. Despite these general side effects of all SSRIs, there are multiple brands of SSRIs. This means that the consumer has the option to pick which medication works best with their symptoms. In the 5-HT4 receptor agonist, however, some of the adverse side effects, like loss of libido, that are seen in SSRIs are speculated to not be present. More research needs to be done with regard to the specifics of the side effects. Despite most of the side effects being unknown, it is known that the 5-HT4 receptor agonist are associated with atrial arrhythmias. Also the 5-HT4-receptor agonist is used as a treatment of gastrointestinal motility, which depending on pre-existing conditions could or could not be a problem.
Although the 5-HT4 receptor agonist seems like a wonder drug, the association with atrial arrhythmias could be a worse side effect than potential for sleeping problems and low libido. However, with the potential for increased risk of suicide as seen sometimes SSRIs, the 5-HT4 agonist could be a better solution. Both SSRIs and the 5-HT4 agonist have an ability to treat depression on two different time scales. However, without more research into the exact side effects of the 5-HT4 receptor agonist, no one can make a confident call on whether this new type of treatment will actually be a better choice than the common SSRIs.

When stressed, many people eat less, citing lack of time or simple forgetfulness as the reason they skip meals or eat less often when they have looming deadlines. What if, when stressed, people get less enjoyment out of their meals? Recent studies have shown that taste disturbances resulting from anxiety or depression may play a role in lower appetite. When we are anxious, we simply cannot taste food as well as we normally would.

Until the last 20 years or so, taste thresholds were thought to be invariable; genetics determined taste threshold, meaning people could range anywhere from a non-taster to a supertaster. Surprisingly, it has come to light that taste thresholds are far more plastic and variable than previously thought. In the first research studies on taste in depressed patients, it was found that depression resulted in decreased sensitivity to all tastes, but to sweet tastes in particular. Those with panic disorder and average people with induced stress tend to be more sensitive to bitter tastes. These taste disturbances seem to be linked to alterations in serotonin (5-HT) and noradrenaline (NA). 5-HT and NA alter ion channel function, resulting in a change in the excitability of taste cells. As a result of this research, in a 2006 study, Heath et al focused on 5-HT and NA in an attempt to determine the link between these monoamines, mood, and taste.

Heath et al studied taste responses to sweet, bitter, salt, or sour tastes in subjects who had no previous history of depression or anxiety and who were not using psychotrophic medication. Taste perception was measured before and after administration of a 5-HT reuptake inhibitor (SSRI, a common ingredient in antidepressant and anti-anxiety medications), a NA reuptake inhibitor (NARI, which treats depression), or a placebo (lactose). Findings indicated that SSRIs significantly increased bitter and sweet taste sensitivity (i.e. these taste thresholds were reduced), while NARIs increased bitter and sour taste sensitivities. Interestingly, neither drug affected salt taste.

So how exactly can SSRIs and NARIs modulate taste? In an earlier model, part of the mechanism was proposed, with additions by Heath et al. First, receptor cells release ATP (which can function as neurotransmitter) as a result of increased intracellular calcium. Next, ATP activates receptors on presynaptic cells, causing an increase of calcium in presynaptic cells, followed by 5-HT release. Heath et al further suggest that serotonergic feedback from presynaptic cells to receptor cells occurs. The 5-HT released from presynaptic cells binds to receptors on the receptor cells, exerting its effects by volume transmission. SSRI administration blocks 5-HT transporters on both receptor and presynaptic cells and enhances 5-HT signaling, and therefore enhances bitter and sweet tastes. On the other hand, NA can act either as a transmitter released onto gustatory afferent axons or by modulating the action of ATP.

In addition to taste perception due to monoamine manipulation, Heath et al studied the relationship between taste and mood. Although all subjects were in the clinically healthy range for Spielberger State and Trait questionnaire (which represent anxiety levels) and Beck's Depression Inventory, some subjects scored on the high range of the Spielberger Trait questionnaire, meaning that they had higher anxiety levels than the other subjects. The more anxious subjects had lower taste sensitivities to bitter and salt tastes. All patients scored very low on depression, so a relationship between depression and taste perception could not be determined. Since 5-HT or NA manipulations do not alter salt thresholds, this effect would need to be studied further.

The next time you get stressed out, think about whether your food seems to taste different than it normally does.

Main article: http://www.jneurosci.org/content/26/49/12664.full.pdf+html