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My Abstract of "Serotonergic Function, Two-Mode Models of Self-Regulation, and Vulnerability to Depression"
The basic focus of this research was to see if low serotonergic function has an effect on executive control, behavior, depression, and aggression. The study also recognizes and tests other aspects of the person’s make up and genetics. The position of the researchers studying this is that those dealing with depression have deficits in executive control, leading to impulsivity, and overwhelming negative emotions.
The article starts off talking about two-mode models of functioning in people. The interplay between these two systems has been related to impulsivity and emotional processing. Basically, there’s the reflexive and the reflective system. People perceive the world through these two different filters. Often times, although they are quite different, people have experiences through them simultaneously. The reflexive system is the “hot” system which is highly emotional and impulsive. The reflective system is the “cool” system which is strategic, slower, and less emotional. For the most part, these two-mode models are in the field of personality psychology. This is all based on the theory that people perceive “reality” and act through two different systems. These systems are important to understand because depending on which one is more dominant, it predicts the way a person will respond and react in a difficult situation.
The article next transitions into the behavioral implications of the two-mode models. It talks about how they have different influences on one’s behavior. This really begins to tie into the overall focus of the article by discussing how behavior dictated by the reflexive system tends to be more impulsive.
Once the two-mode model theory is explained, the article starts delving into the physiological and biological aspects of the study. A large part of the research starts to examine the amygdala and how it and how it ties into all of this. As it turns out, the amygdala plays a very large role. It puts emotional value onto stimuli and decides the amount of reaction that is merited. Different sub cortical areas begin to be looked at and it was found that they are also found to have a part in emotional processing and play into impulsive action. In a study that the article briefly mentioned, it was found that there is a level of higher activity in the amygdala and other sub cortical areas in killers that had been convicted of impulsive murders.
Once the article laid out all of this basic foundation for its premise, it started to really focus in on its target. It began to discuss the methods of human research on serotonergic function. Serotonergic function links into the two-mode models because it influences the balance between the two. When it comes to the way serotonergic function operates in the nervous system, there are still a lot of questions and not a whole lot has been explained. The researchers move on to explain that while they suspect that serotonin levels have a large influence on their topic, there’s much more involved. They discuss other factors, such as; the efficiency of metabolizing neurotransmitters that are released into the synaptic cleft, sensitivity and density of receptors, efficiency of reuptake of neurotransmitters from the cleft, the recent history of cell’s firing, and the person’s dietary intake of amino acids.
The article then moved into talking about acute Tryptophan depletion and enhancement. This is a very common and direct procedure. What happens is the people participating take capsules (or drink) containing high levels of about fifteen amino acids with no Tryptophan. What this does is it depletes the person of Tryptophan. Tryptophan is a precursor to serotonin. The manipulation result is an episode of Tryptophan depletion that takes place a few hours after the people take the capsules. It was found that the strongest effect of Tryptophan depletion was found in people that were regarded as being highly impulsive, which is consistent with the theory of two-mode models. What was very interesting was that in one experiment, Tryptophan depletion (in females) led the participants to show slower processing of happy words, but not sad words. It was found that generally Tryptophan depletion didn’t have a very large effect on those without a family history of depression. However, it really did exaggerate mood change when the people were put in a situation with a stressor. It also led the people to feel much sadder when they were exposed to an uncontrollable stress such as aversive, excessive noise. Then, people who were assed as having high aggressive tendencies became more aggressive, hostile, and quarrelsome. Then the researchers studied the participants after enhancing their Tryptophan. The people that had been so aggressive and hostile before had become much more calm and docile.Another way researchers study this is by using a drug called fenfluramine. By using Fenfluramine researchers can do tests for different types of aggression.
The article then started to discuss the genetic part of the research. It related the behaviors they were studying to genetic polymorphisms that have most definitely been independently associated with serotonergic function. They examined the gene that codes the serotonin transporter. Having information on these transporters is extremely influential to their research of this topic because the transporters play a very important role in serotonergic transmission by facilitating reuptake of serotonin from the synaptic cleft. They have found a polymorphism called 5-HTTLPR; there is a short version and a long version of this allele. Quite a bit of evidence has been found that links this polymorphism to serotonergic function. The short allele has quite different affects on the person’s behavior than the long allele. There was a study recently performed that showed that carriers of the short allele had twice the turnover of serotonin in their brains as people with the long allele of this polymorphism. Psychologists and scientists all over have found that the short allele is a clear flag of low serotonergic function. They have linked the short allele to an elevated risk of depression. Thus, there seems to be solid evidence that connects low serotonergic function to depression. As it turns out, genetic and physiological things such as polymorphisms really can have an effect on aggression and depression.
The article then moved on to explain how everything that has been discussed thus far has relevance to their stance that serotonergic function has an effect on depression and impulsive aggression by going over the relationship between serotonergic function and the brain. To oversimplify completely, the (central) main serotonergic system comes from the brain stem and goes throughout cortical and suboptimal structures. When it comes to the functioning of cortical structures, serotonin is very important. Cortical and sub cortical structures in the brain are all interconnected and regulate emotion and behavior. In your brain there are different neural circuits and one of these circuits is called the corticolimbic neural circuit and what it does is mediate emotion. It’s densely innervated by serotonergic neurons and has a lot of serotonergic receptors. There is a very strong, established theory that serotonin is critical in the development of emotional circuitry. It’s particularly involved ion constraining excitatory influences when it comes to the amygdala. This begins to tie into the research done on the 5-HTTLPR polymorphism I mentioned earlier because people who carry the short allele of this polymorphism have a greater amygdala reactivity to averse emotions. The prefrontal cortex is the area of the brain that constrains amygdala activity. The prefrontal cortex area has the most serotonin transporter terminals in the entire human cortex and is the target of projections from the amygdala. Overall, this entire circuit is affected by serotonergic function.
After all of this is understood, the article moves into talking about cognitive and behavioral effects of serotonergic function and how serotonergic function and emotion have related processing. High serotonergic function basically facilitates cognitive and behavioral inhibition when it comes to peoples’ emotional states and impulses.
The article then moves into discussing conduct disorder, personality disorder, and violence. They found that conduct disorder and antisocial displays were linked to a basic lack of executive control and they also linked all of that to serotonergic function by experimenting with the drug fenfluramine. It was found that lower serotonergic function is linked to violence and impulsive aggression. Coming back to the genetic evidence dealing with the short allele of the polymorphism 5-HTTLPR; the polymorphism is related to traits dealing with borderline personality disorder and antisocial personality disorder. Some genetic evidence heavily links serotonergic function to violent and antisocial behavior. The article discussed a study of a sample of men in China that had been convicted of extremely violent crimes. They concluded that the aforementioned men were indeed carriers of the short allele of 5-HTTLPR. Such researchers as McDolan, Anderson, and Deacon were discussed and they had all found that in their experiments they had been able to link low serotonergic function to higher impulsivity and higher aggression in male aggressive offenders. Both impulsivity and aggression also were related to higher anxiety. They then began to discuss the relationship between lower serotonergic function and psychopathy. They found that lower serotonergic function does not mean overall psychopathy but it does relate to impulsivity, a component to antisocial disorders, which puts together irresponsibility, impulsiveness, and overall poor behavioral control. Certain evidence has found a patter that suggests problems constraining emotion in the circuitry; there are impairments in people assessed to be antisocial in their dorsolateral and orbito frontal regions of their prefrontal cortex, amygdala, and interior cingulate.
Suicidal acts are largely tied to impulsive aggression and serotonin metabolites in cerebrospinal fluid. There have been cross-sectional studies done that suggests that the serotonin metabolite 5-HIAA is related to greater lethality of suicide attempts.
The connection between personality traits and serotonergic function is then discussed. In non-clinical samples hostility (as a trait) has been related to low serotonergic functions. When it comes to personality, it seems that low serotonergic function relates most strongly to irritability and assaultiveness as opposed to passive forms such as resentment and suspiciousness.
In conclusion, after I was finished reading this article I was left with the strong impression that serotonergic function does, indeed, have a strong connection between depression and aggression.
There was a certain part of this article that really sparked my interest and got me asking questions. The article very briefly began to discuss the effects gender has on depression. It said that some studies have raised the idea that perhaps the effects of low serotonergic function depend partly on interactions of serotonin with sex hormones since women are nearly twice as likely as men to experience clinical depression. That got me really wondering about that and I think that an investigation of that question would be very interesting and beneficial.