Shining a Light On A Truly Brave, New World

There is a tide in the affairs of men
Which, taken at the flood, leads on to fortune;
Omitted, all the voyage of their life
Is bound in shallows and in miseries.
On such a full sea are we now afloat,
And we must take the current when it serves,
Or lose our ventures. _JuliusCaesar (IV.ii.269–276)

Sometimes the difference between success and disaster hinges upon a small decision. But making hard decisions requires courage -- or does it? Perhaps the requirement for making tough decisions is the ability to overcome the anxiety and fear that decision-making often entails? And the key to overcoming anxiety and fear may be as close as the nearest light source.

"I've never seen anything like it," says Kay Tye, a postdoctoral researcher in Deisseroth's lab and lead author on the study. Mice are naturally fearful of exploring open areas, she explains. Under normal circumstances, the animal "will poke its nose out and then scurry into a corner," says Tye. "But when you turn on the light, the animal begins exploring the platform with no visible signs of anxiety. Then you turn the light off, and it scurries back in to the corner."

...The researchers engineered mice to express light-sensitive proteins in specific cells in the amygdala that send out neural wires, known as axons, to different substructures. Using a specially designed fiber-optic cable implanted in the animal's brain, researchers found that aiming the light to activate one specific circuit had an immediate and potent effect on the animal's behavior.

..."Our understanding of the more precise circuitry within the amygdala is just now beginning to take off," says Kerry Ressler, a neuroscientist at Emory University who was not involved in the study. "Optogenetics, where scientist can activate specific cell populations and even parts of cells, is a powerful approach to dissect how the amygdala modulates fear and anxiety."

Ki Ann Goosens, a neuroscientist at MIT who was not involved in the study, says the research could help explain individual variation in baseline anxiety levels. "The findings tell us that this circuit contributes to an individual set point for anxiety," she says. _TechnologyReview

Tiny brain circuits can make all the difference in a person's life. A society comprising fearful, anxious, security - fixated persons, will have a far different destiny than a society made up of of imaginative, thoughtful, and courageous persons.

Perhaps it is no accident that most western societies find themselves clinging to present security at the expense of their own futures. That is the way of a cringing and shrinking death at one's own cowardly hands.

Besides a mastery of fear and anxiety, persons will also require wisdom and logical thinking skills, if they wish to catch the tide at its flood, sailing on to fortune. Logic must have both courage and wisdom, or it will be left either paralysed, or will find itself a force of wasted -- or even destructive -- effort.

Research can only reveal tiny, disconnected pieces of the current conundrum. But an integrated solution requires a wider-ranging mind than one finds in most lab rats, dependent on government funding and constraints of all kinds. Rather than huddling together in institutions and special-interest lobbies and unions, people of the next level will require courage, wisdom, logic -- and competence.

One must not only know what needs to be done when, and have the courage to do it, but also know how to do it properly and effectively.

Feeding Stress: Sweet-Cycling the Amygdala

The central amygdala is involved in fear, stress, and anxiety responses. Researchers at Scripps have discovered that the central amygdala's stress response is elevated 5X when a dieter accustomed to sweet foods is switched to normal chow.

"We found that rats cycled in this way between palatable food and less tasty, but otherwise acceptable, food, begin to binge on the sweet food, stop eating their regular food, and show withdrawal-like behaviors often associated with drug addiction. As in addiction to drugs or ethanol, the brain's stress system is involved in each of these changes."


...the researchers looked at the involvement of the brain's stress system -- which had been shown to contribute to patterns of drug and alcohol binging and withdrawal -- in underpinning these behaviors.


To do this, the team measured levels of stress-related corticotropin-releasing factor (CRF) mRNA and peptide in an area of the brain known as the central amygdala, which is involved in fear, anxiety, and stress responses. Indeed, the researchers found that the diet-cycled group on normal chow displayed five times the control group's levels of CRF. Only when the diet-cycled group was fed sweet food did CRF levels return to normal.


"CRF is a key stress neuropeptide," said Cottone. "In observing the activation of the amygdaloid CRF system during abstinence from sweet foods, we understood the causes of recurrent dieting failures."


...To confirm these results and to see whether blocking CRF could reverse some of the effects of diet cycling, the researchers turned to a compound called R121919 (a small molecule CRF1 receptor antagonist).


When administered to the diet-cycled rats, the compound blunted the bingeing on sweet chow, as well as the lackluster pursuit of regular chow and the anxiety-associated behaviors during this part of the diet cycle. As in similar studies modeling alcoholism, on a molecular level diet-cycled rats showed greater sensitivity to the ability of the CRF1 receptor antagonist to reduce central amygdala synaptic transmission of the neurotransmitter GABA, which plays an important role in regulating neuronal excitability. _SD

Very interesting.   High levels of stress underlie many addictions.  Of course, these are rats, not people.  It looks as if the same sort of CRF receptor blocker can blunt addictive behaviours in humans -- to foods, drugs, and other dysfunctional behaviours. We might soon see 13 step anti-addiction programs opening up.  The 13th step would be the use of CRF receptor bloockers.

Do you think they could put those blockers in ice cream?

Soothing A Distressed Brain: FGF2

Anxiety (40 million American adults) and depression (15 million American adults) are among the most common causes of disability and academic failure / underachievement worldwide. If one were to develop an effective, safe, and non-addictive treatment for anxiety and depression, the positive impact on the human world would be immense. University of Michigan researchers have studied the impact of FGF2 -- fibroblast growth factor 2 -- in 19 generations of rats that were bred selectively for high or low anxiety levels.

"We have discovered that FGF2 has two important new roles: it's a genetic vulnerability factor for anxiety and a mediator for how the environment affects different individuals. This is surprising, as FGF2 and related molecules are known primarily for organizing the brain during development and repairing it after injury," Perez said.

Finally, the findings suggest that part of FGF2's role in reducing anxiety may be due to its ability to increase the survival of new cells in a brain region called the hippocampus. Previous research has suggested that depression decreases the production and incorporation of new brain cells, a process called neurogenesis. Although the researchers found that high-anxiety rats produced the same number of new brain cells as low-anxiety rats, they found decreased survival of new brain cells in high-anxiety rats compared to low-anxiety rats. However, FGF2 treatment and environmental enrichment each restored brain cell survival. _Genengnews

Persons with chronic anxiety and depression may also have significant memory problems, perhaps due to reduced neurogenesis and reduced survival of new brain cells. Treatments that allow new cells to survive and function normally in the brain would logically help to normalise the life experience of persons with chronic anxiety and clinical depression, and reduce the enormous societal expense of these mental health disorders.

Fear, Anxiety, Depression: One Puzzle Piece

Current therapies for depression and anxiety disorders are less than perfect. When the potential for new and effective therapies for mental health disorders appear, it is cause for hope and scrutiny. Acid Sensing Ion Channel protein (ASIC1a) plays a key role in the experiencing of fear, prolonged anxiety, and depression. Researchers in Iowa have studied this protein for over two years, and earlier demonstrated that disrupting ASIC1a blunts the "fear response" of mice. Now, the Iowa researchers have demonstrated an anti-depressant effect in mice by blocking the ASIC1a protein.

The UI research team found that disrupting ASIC1a -- an ion channel protein found in the brain -- produced an antidepressant-like effect in mice. The effect was similar to that produced by currently available antidepressant drugs, but the team also showed that ASIC1a's effect arose through a new and different biological mechanism. _PO

This approach to the study of anxiety and depression promises to bring about entirely new therapies for these disorders. Several years are likely to pass before ASIC1a-based treatments are on the market, but given the growing costs of mood and anxiety disorders to health care systems around the world, useful leads for researchers to follow can only help.

In the meantime, large numbers of pharmacological and non-pharmacological treatments for anxiety and depression are available.

30 Top Resources for Non-Pharmacological Therapies for Depression

Guest post by Kat Sanders

Depression is not something that we can take lightly; it may start out as a mild form of sadness, but if left untreated or unmanaged, it could turn into a full blown mental disorder that causes more complications than you can handle. Rather than resort to drugs to treat depression (they come with a host of side effects and are sometimes addictive), you could try these top resources for non-pharmacological therapies for depression. A word of warning - these are not meant as professional advice, so consult your doctor before you stop your medication or try something new.

There are various alternative methods of treating depression, and some of them are:

Psychotherapy: this is a method that uses cognitive behavior therapy and other coping strategies to help deal with their problem. A few sites that have good information on psychotherapy are:

• About.Com s Depression and Psychotherapy page


• Psych Central s resources on psychotherapy


• Psychotherapy Resources offers depression help in North Carolina and in general


• Patient.Co.UK has information on psychotherapy and related resources in the United Kingdom


• Psychotherapy.Net links to articles and interviews with qualified therapists who deal with depression on a daily basis.


• Anxiety Insights offers information and news on psychotherapy, depression and related topics.

Light Therapy: is used to help people who suffer from depression because of living in houses where there’s not enough natural light and in places where sunlight is missing for the major part of the year. It involves being bathed in artificial light for at least half an hour each day. Below are a few sites that offer comprehensive information and resources about this therapeutic method.

• Light Therapy Australia contains access to resources on light therapy down under and in general.



• Light Therapy Products lists products that help you cope with and prevent depression that’s induced by a lack of natural light


• Holistic Online s light therapy page contains information on this disorder


• Pscyeducation.Org tells you more about light therapy


• Mayo Clinic’s pages on light therapy and seasonal affective disorder (SAD) offer you more information on these conditions



• Full Spectrum Solutions offers links to products that help prevent SAD and suggestions and ideas for full spectrum lighting

Aerobic Exercise: Cardio workouts that get your heart beating have been proven to be mood enhancers and are thus a great cure for depression. Regular exercise releases endorphins and other feel good chemicals that keep you in good spirits the natural and healthy way. Some sites that offer quality resources on exercising and beating depression are:

• Mental Health UK lets you access resources on health and exercising


• Hub Pages tells you how exercise keeps depression away


• Buzzle.Com features an article on depression, exercise and stress


• Natural Cures for Depression shows you how to beat depression using exercise



• Articles Base has various articles on exercise and depression


• The Uplift Program offers products to help you chase away the blues by exercising

Supplements: From time immemorial, people have been using herbs and other natural substances to treat depression and other mental disorders. A few sites that offer information on supplemental treatment for depression are:

• Helium.Com tells you what you need to know before you use herbal supplements to treat depression


• I Love India offers a list of herbs that help in treating depression


• Native Remedies tell you how various herbs work in helping you cope with depression



• Buzzle.Com provides two great articles on how to treat depression with herbs and why you can depend on them to beat depression away


• Treat Depression Naturally offers you tips on the herbs that work in treating depression


• EHow.Com offers advice on using herbs to help with depression

Foods: Some foods are known to be great mood enhancers because of the chemicals they contain, like chocolate. If you want more information on foods that boost mood and help people who are depressed, check out the below list:

• Natural News offers a list of food groups that help beat depression



• Search Warp tells you why certain foods help enhance your mood and chase away depression


• Ezine Articles offers information about foods that are supposed to keep you upbeat


• Jared Story tells you why food therapy is good for treating depression


• Ayush Veda also tells you why you must eat certain foods to keep your spirits up



• Web MD offers a list of foods that help beat winter depression

By-line:

This article is written by Kat Sanders, who regularly blogs on the topic of MRI technologist schools at her blog MRI Tech's Health Blog. She welcomes your comments and questions at her email address: katsanders25@gmail.com.

Visualizing Intelligence & Genetics of Fear

Brain imaging is improving so quickly that soon we may be able to measure intelligence using brain scans, and simply skip the IQ tests altogether.

... lesions in the left frontal cortex were associated with lower scores on the verbal comprehension index; lesions in the left frontal and parietal cortex (located behind the frontal lobe) were associated with lower scores on the working memory index; and lesions in the right parietal cortex were associated with lower scores on the perceptual organization index.

Somewhat surprisingly, the study revealed a large amount of overlap in the brain regions responsible for verbal comprehension and working memory, which suggests that these two now-separate measures of cognitive ability may actually represent the same type of intelligence, at least as assessed using the WAIS.

The details about the structure of intelligence provided by the study could be useful in future revisions of the WAIS test so that its various subtests are grouped on the basis of neuroanatomical similarity rather than on behavior, as is the case now.

In addition, the brain maps produced by the study could be used as a diagnostic aid. Clinicians could combine the maps with their patients' Wechsler test results to help localize likely areas of brain damage. "It wouldn't be sufficient to be diagnostic, but it would provide information that clinicians could definitely use about what parts of the brain are dysfunctional," Adolphs says.

The converse--using brain-scan results to predict the IQ of patients as measured by the Weschler test--may also be possible. Although the results wouldn't be as clear-cut as they are in patients with brain lesions, Adolphs says, "you could take a large sample of healthy brains and measure the relative volumes of specific brain areas and draw some associations with these IQ factors." _Eurekalert

This study used scans of persons with brain lesions to correlate with Wechsler test scores. Future brain scans will reveal far more detail anatomically and functionally. As spatial and temporal resolution of brain imaging improves, the newer brain imaging should provide far more insight into the neural correlates of intelligence.

On another topic, research into the neuroscience of fear is revealing the importance of genetic polymorphisms in the experience and recovery from fear and anxiety in everyday life.

The results showed that while the participants with the shorter version of the serotonin transporter gene developed a very strong physiological fear response to picture A, participants with a longer version of the gene did not. In addition, a variation in the gene coding for the COMT enzyme was associated with fear extinction - volunteers with this particular variant were able to very quickly overcome their fear while volunteers with the other variant failed to do so.

The researchers note that these findings have very interesting implications for understanding gene-environment interactions and that "genes may act through the environment by making carriers of particular gene combinations more likely than other individuals to easily pick up and retain fear of stimuli associated with threat and trauma." The authors go on to suggest that these findings may indicate that individuals with specific polymorphisms may be more susceptible to anxiety disorders by being more prone to developing fear and being less likely to overcome that fear by common cognitive behavioral treatments which are based on the extinction principle. _SD

We are all unique in our responses to our different environments. While some are certainly predisposed genetically to experience more fear and anxiety in response to ordinary everyday experiences, we should all be allowed to learn how to overcome fear and anxiety responses in order to be able to pursue our life's goals. In the absence of such training to overcome innate anxiety responses, individuals can be prone to obsessing on perceived external obstacles to success. Such obsession on externals makes it almost impossible to understand the far more important internal obstacles to reaching satisfactory plateaus of achievement.

Brain Stimulation Preserves Brain Cells, Zen Training Restores Distracted Attention

In Parkinson's disease, certain dopamine secreting cells in the substantia nigra die off, leading to the loss of fine control of motion. But deep brain stimulation with implanted electrodes in the brains of rats preserves dopamine cells by causing increased levels of BDNF (brain derived neurotrophic factor), suggesting a similar therapy in humans may halt progression of Parkinson's. Remember that BDNF can also stimulate the differentiation of neural stem cells into mature neurons.

During the DBS study, researchers implanted high-frequency stimulating electrodes in the subthalamic nucleus, an area of the brain associated with movement, in rats and then induced dopamine neuron loss. When the rats had experienced a 50 percent loss of dopamine neurons, the researchers initiated brain stimulation in half of the group. Measurements of surviving, functioning dopamine neurons in rats implanted with active stimulators were then compared to a control group implanted with inactive stimulators. While the control group’s loss of dopamine neurons increased to 75 percent after two weeks, the rats implanted with active stimulators experienced no further loss of cells during that time.

Subsequent tissue analysis revealed that in rats implanted with active stimulators the trophic factor BDNF had tripled in the striatum, a part of the brain that houses dopamine terminals and “receives” the dopamine neurotransmitters that are produced in the substantia nigra. _SD

In other research, it was found that persons with Zen training are able to refocus their attention more quickly after being distracted, than persons without such training.

The study compared 12 people from the Atlanta area with more than three years of daily practice in Zen meditation with 12 others who had never practiced meditation...While having their brains scanned, the subjects were asked to focus on their breathing. Every once in a while, they had to distinguish a real word from a nonsense word presented at random intervals on a computer screen and, having done that, promptly "let go" of the just processed stimulus by refocusing on their breath....

After interruption, experienced meditators were able to bring activity in most regions of the default network back to baseline faster than non-meditators. This effect was especially prominent in the angular gyrus, a region important for processing language. _SD

Scientists have also created an animal model of chronic stress by boosting levels of corticotropin releasing factor (CRF) in a specific part of an animal's brain. Drugs to modify the effect of CRF in humans have been in the pipeline for some time. Perhaps eventually a non-addictive treatement for chronic anxiety and over-stress will be developed. Meditation, exercise, and avoiding bad habits can also do wonders.

Remember the wonder drug Dimebon, being studied as a treatment for Alzheimer's? Pfizer has acquired the rights for the drug from Medivation. Scientists are also beginning to zero in on the specific protein-protein interactions that lead to damaging neurodegeneration in Alzheimer's, Parkinson's, Huntington's, etc.

Here's a report of more research into stimulating replacement neurons in the brain for treating neurodegenerative disorders.

Remember: All of this research is made possible by the excess wealth generated by market economics. The more of that excess wealth (profit) that government sucks up through taxation, or prevents by excess regulation or counter-productive tort laws, the less research that can be done. Government and foundation funding through NIH etc. is only possible when there is excess wealth available to begin with. Have you ever wondered why most of the research is being done in non-socialist countries?

Serotonin Receptor Agonists: Better than SSRI's?

Serotonin has been shown to be important in depression and anxiety. But what is the best "serotonin approach" to treating depression? SSRIs (selective serotonin reuptake inhibitors) such as Prozac are generally effective, but may take several weeks to achieve maximum effect. Another approach is for a drug to directly stimulate serotonin receptors--serotonin (5HT) agonists.

Recent research into 5HT4 receptor agonists, using rats as subjects, appears to promise faster and more efficacious serotonergic antidepressants.

Antidepressants that directly enhance serotonin signaling appear to have a much faster onset of action in animal models of depression than selective serotonin reuptake inhibitors (SSRIs), said investigators here.

Rats given one of two serotonin -- (HT4) agonists -- a new class of drug-showed behaviors and brain changes within three days that were suggestive of antidepressant effects that would take two to three weeks to achieve with an SSRI, reported Guillaume Lucas, Ph.D., of McGill University, and colleagues in the Sept 6 issue of Neuron.

The authors provide "and extensive and convincing data set" suggesting that this new class of molecules is fasting-acting and potentially efficacious, but whether they will see the light of day as therapies for human depression is still unknown, cautioned Ronald S. Duman, Ph.D., of Yale, in an accompanying editorial.

"These agents will require extensive testing in clinical trials for confirmation, because of limitations inherent in rodent models of depression and antidepressant response and because of potential side effects," Dr. Duman wrote.

Source

The important thing to remember is that although some humans may behave like rats, humans are not rats. Research on models of depression in rats may not transfer directly to good results in humans. Drug safety in humans and drug safety in rats are certainly not the same, either.

In an area of therapeutics such as depression, regulatory agencies will likely require extensive clinical studies before approval. It is important to point out, however, that depression is a potentially fatal disease. Any drug that promises rapid emergence from deep clinical depression, and which is also safe for short to intermediate term use, may find an important function in the treatment of depression--even if it is not approved for long term use.

This is an interesting result of the study:

They found that the action of the drugs on the 5-HT4 receptor "deeply modified" serotonin transmission by enhancing firing of dorsal raphe neurons in the hippocampus. In addition, three days of treatment also significantly promoted neurogenesis in the subgranular zone of the dentate gyrus of the hippocampus, an effect normally seen after a minimum of two weeks of treatment with classical antidepressants or SSRIs.

If depression kills neurons, and effective antidepressant therapy promotes new neuron growth, the new approach to stimulating serotonin receptors appears to do its formative work on neuronal stem cells more quickly than SSRIs.

Forms of Anxiety: Apprehension vs. Arousal

One of the major failings of Psychiatry is that it is unable to differentiate between mental disorders of different etiologies that produce similar symptoms. One form of anxiety, for example, is not the same as another--and the treatments should reflect the differences in etiology.

The DSM classifications lack the fine discrimination that neural-genetic etiology could provide. But neuro-reasearch is slowly providing psychiatry with the background knowledge that it has been lacking for so long.

The researchers used functional Magnetic Resonance Imaging (fMRI) to map the brain areas with heightened neural activity during a variety of psychological probes.

As the researchers had predicted, the anxious apprehension group exhibited enhanced left-brain activity and the anxious arousal group had heightened activity in the right brain. The anxious apprehension group showed increased activity in a region of the left inferior frontal lobe that is associated with speech production. The anxious arousal group had more activity in a region of the right-hemisphere inferior temporal lobe that is believed to be involved in tracking and responding to information signaling danger.

Source

While EEG had localized apprehension to the left brain and arousal to the right brain, fMRI was able to further localize apprehension to the left inferior frontal lobe and arousal to the right inferior temporal lobe. This distinction is extremely important for the study of the different anxiety disorders, and eventual treatments.

Consider deep brain stimulation treatments, for example. Being able to place electrodes in the precise location for the precise disorder should be more efficacious than uniform placement for all disorders within a broad classification.

Remember: Be Afraid--Be Very Afraid, Monsieur Amygdala

The amygdala is involved in fear and fear based memory. A recent article at the Neurophilosopher Blog provides a fascinating discussion of the general role of the amygdala, along with some very interesting recent research findings into gene expression within the amygdala.

The amygdala receives its main inputs from the visual, auditory and somatosensory cortices; it couples these sensory stimuli (something scary) to the fight-or-flight response and, therefore, its main outputs are to the hypothalamus, which controls hormone production and homeostasis, and autonomic centres in the brainstem.

Recent work by Gleb Shumyatsky and his colleagues at Rutgers University in New Jersey has led to the discovery of several genes that are enriched in the amygdala and appear to be involved in the formation of fearful memories. One of these proteins, stathmin (also known as oncoprotein 18) is now known to be involved in mediating the formation of memories of of both conditioned and unconditioned fear; there is a high level of expression of the stathmin gene, and a corresponding high concentration of stathmin protein, in the amygdala, but not in the adjacent hippocampus.

Mutant mice lacking the stathmin gene were unable to learn new fears or to act instinctively in a fearful situation, i.e. they had weaker memories of fearful experiences. The stathmin knockout mice also showed less anxiety when presented with new mazes to explore or with potentially dangerous situations. Upon further examination, it was observed that mice lacking the stathmin gene had a less dynamic microtubule network than wild type (normal) mice. Memories are formed by the establishment of new synaptic connections, which require a re-arrangement of microtubules. In the absence of the stathmin protein, microtubules aren’t re-arranged so easily, and, as a consequence, the synapses that would normally be modified during memory formation are not as plastic as they should be.

More recently, researchers have used functional magnetic resonance imaging (fMRI) to show that the rostral anterior cingulate cortex(rACC) modulates activity in the amygdala, effectively acting as an ‘on-off’ switch. Joy Hirsch and her colleagues at Columbia University used a variant of the Stroop test, which involves presenting words for colours, which are printed in a colour that differs from that of the meaning of the word (e.g. green). This discrepancy leads to a delay in the processing of the visual information, reducing the reaction time taken to perform the task.

Instead of using words, Hirsch’s team presented participants in their experiments with photographs of happy or scared faces with the word ‘HAPPY’ or ‘FEAR’ written across them. It was found that the amygdala was activated before the rACC when the participants were presented with a happy face with the word ‘FEAR’ printed across it. Soon afterwards, though, the activity in the amygdala would be reduced. That is, initially, the amygdala processes the word ‘FEAR’, but, soon afterwards, the rACC processes the happy face, and inhibits activity in the amygdala to reduce the fear response. In contrast, when participants were presented with a photograph of a scared face which had the word ‘FEAR’ written across it, the rACC remained inactive, while activity in the hippocampus persisted for longer.

More at Source.

In twin studies, some aspects of phobia show a heritability of around 45% or higher.

Although many social scientists still deny the importance of heritability in cognitive and emotional function, people who actually work in the field know better. In fact, it would not be surprising to find that heredity influences cognitive styles that would predispose individuals to particular styles of political or ideological belief, within the broad spectrums of human political/ideological behaviour.

When one contemplates the increasing likelihood that different attitudes toward morality are at least partially inherited, it is not a great leap to expect that heredity plays a part in philosophical, ideological, or political predisposition. Teasing out all the possible mechanisms will be beyond complex.

Why so Afraid, Little Flower? Is it your Amygdala Again?

We are all at the mercy of our genes. Your genes determine the color of your eyes, your hair, your approximate height, and much of your personality. Are you sanguine? Are you cheerful? Are you fearful? Activation of your amygdalae has a lot to do with serotonin levels in synapses, and the level of negative emotions you experience. Serotonin levels in the synapse are largely determined by your genes. "How Genes Make up Your Mind" is an interesting article in the Science and Consciousness Review.

Genes control the development of neurons to make up brains, but they also govern neuronal gene expression during our daily lives. The sleep-waking cycle is controlled by neurochemicals emerging from cells at the base of the brain. Genes control how neurons communicate with serotonin, dopamine or other neurotransmitters (cache). Genes are responsible for every step of the neurotransmitter cycle, including the formation, transport, pre-synaptic expression and post-synaptic reception of the transmitter (see Figure 1). Genes work at every level of the neural process. They are the fundamental building blocks for both the structure and the functioning of the brain.

....How do genes influence the emotional workings of brains? Recent studies now show that naturally occurring genetic variations - called polymorphisms (cache) - which code for serotonin affects our emotional reactions and thoughts. Humans have two common variations of a promoter region of the serotonin transporter gene (5-HTTLPR); a short (s) and a long (l) version. It has been shown that two allelic (cache) copies of the long variant leads to higher concentration of 5-HTT mRNA, which leads to a doubled reuptake of serotonin, compared to one or two short allelic variations. People who have two copies of the long genetic sequence in this region have less serotonin available in the synapse, due to the higher reuptake of the neurotransmitter.

....The researchers found that the actvation of the two amygdalas differed between the two groups (see Figure 4). The s group showed a significantly higher amygdala activation than the l group. In other words, the level of amygdala activation depended on what genetic makeup a person had. Having a short version of the 5-HTT genetic code leads to a higher level of synaptic serotonine, which again leads to a higher level of amygdalar response to aversive stimuli. This is consistent with the prediction described above.

While these results have provided us new information about how genes regulate brain function, one can ask: does this have any effect on thought and behaviour? Indeed it has! Studies demonstrate that carriers of the s allele, compared to l allele carriers, are more likely to show abnormal levels of anxiety (5) develop affective illness (6) and even acquire conditioned fear responses (7). Variations in the genetic makeup of the serotonin system has profound influence on our experience and behavior. Thoughts are shaped by genes.

The original article contains several useful links. Check it out.

Not everyone wins the genetic lottery. At least now we are beginning to understand what happens, and what might be done to bring the advantages of good genes to the amygdalas of everyone.