The Role of Inhibitory Signals in Antisocial Behavior

The term "Running around like a chicken with its head cut off", has deeper meaning when discussed in the context of the nervous system. When a chicken's head is cut off from its body, the body of the chicken still retains the ability to run around for a period of time before it expires. By disconnecting the head from the body, one has essentially turned off the inhibitory signal that keeps the chicken from running around. As humans, it also seems as though we are continuously being inhibited from performing actions. If the brain is equal to behavior, then the turning on or off of these inhibitory signals dictates who we are and how we behave. But how do inhibitory signals affect behavior in humans? At some level all humans must have the same level of inhibitory signaling because we all perform similar basic functions. However individuals can deviate from the "baseline" and exhibit behavior that results from a decrease in the level of inhibition signaling. This can result in antisocial behavior, which can consequently lead to an increased risk of exhibitng aggressive behavior.

In 2002 , a study performed at the University of Wisconsin-Madison, examined the relationship between neurotransmitters and antisocial behavior (3, 5). The study involved a cohort of 442 males from New Zealand, and the study spanned from birth to age 26. The study found that a gene which regulates an enzyme called monoamine oxidase A (MAO A) may be a causal factor of the antisocial behavior of the individuals. MAO A functions to get rid of excess neurotransmitters, and in the study it was found that individuals with low levels of MAO A tended to exhibit more aggressive behavior. Out of the 442 males studied, it was determined that 163 individuals had low activity of MAO A, and these individuals were nine times more likely to exhibit antisocial behavior, such as persistent fighting and lying. However the study found that low levels of MAO A did not produce antisocial disorders in all subjects (3, 5). Therefore it seems that this genetic factor may increase the risk of developing antisocial behavior, but does not guarantee that an individual with low levels of MAO A will develop an antisocial disorder. However, this study does point to a relationship between disinhibition and increased aggressive behavior.

A study presented by Van Goozen et. al in 2008, presented theories as to why individuals with compromised neurobiological systems are at a higher risk of exhibiting antisocial and aggressive behavior. The study examined the relationship between neurobiological systems and antisocial behavior in children (6). In a previous study by Fombonne et al., it was found that conduct problems in childhood have a strong correlation to negative outcomes in adulthood, and may be a strong predictor of conduct disorder in adulthood (2). This study specifically examined the relationship between the stress response system and antisocial behavior; with the hypothesis that individuals that exhibit antisocial behavior are less sensitive to stress; which was deduced from the fact that aggressive individuals place themselves in risky and/ or dangerous behavior more often than other people (6). The stress response systems include the hypothalamic-pituitary-adrenal axis, and the autonomic nervous system; along with the neurotransmitters systems which include the neurotransmitters serotonin, norepinephrine, and dopamine (6).

The study presents two intriguing theories which try to account for individual differences in aggressive behavior (6). The first theory is that aggressive individuals have a low level of fear, which would consequently lead to delinquent behavior (4). This theory is based off of the inference that individuals who exhibit antisocial behavior are compromised in their ability to perceive and process fear and threat due to their compromised neurobiological system (6). In this case the neurobiological systems refer to signals that process threat and predict punishment. Thus because these neurobiological systems are insensitive, antisocial individuals tend to exhibit aggressive behavior more often than individuals who are not considered antisocial. The amygdala is the main part of the brain that is thought to be most involved in the perception of threat or fear from the environment (6). This theory is supported by a previous study performed in 1999 by Bechara et. al, which found that patients with lesions in the amygdala showed deficits in fear conditioning and affective decision making (1).

The second theory claimed that aggressive individuals experience different levels of sensation seeking than individuals who do not exhibit aggressive behavior (7). The theory is based off the claim that some stress is needed to feel pleasure, and that too much or too little stress can have the averse results (6). This theory states that aggressive individuals are under aroused in relation to their stress levels, and also have an elevated threshold for stress. The under arousal theory claims that in antisocial individuals, arousal systems are reduced under conditions when the individual is at rest, or when the individual is performing normal tasks. These physiological changes are associated with the hypothalamic-pituitary-adrenal axis, in addition to other parts of the brain (6).

From these studies, it seems that the relationship between inhibitory signaling and antisocial behavior is not simply a matter of whether an inhibitory signal is turned on or off; but of the relative levels of signaling that occur in the brain. Both studies seem to indicate that disinhibition of neurobiological systems, or lowered activity of these systems, create an increased risk of exhibiting antisocial and aggressive behavior. Lowered levels of activity or compromised function of the neurobiological systems leads to a higher risk of abnormal behavior when compared to individuals that do not have these types of deficits in their neurobiological systems.

These studies try to take account for environmental factors as well, and how genetic predisposition and environment affect the persistence of antisocial behavior. While I consider these theories valid in their account for their relationship between inhibition and antisocial behavior, there are still some ethical and social issues that remain unexplained.

When considering genetic predisposition to a certain type of disorder, several ethical considerations come to mind. For instance, how can research measure the extent to which social factors, such as environment with which the individual was raised, and access to resources within environment, have affected the neurobiological systems of the individual? All individuals respond to situations differently, and it does not seem that a baseline can be assumed when considering emotions and their impact on exhibiting antisocial behavior. Perhaps in some instances, individuals may exhibit low levels of MAO A, or have decreased function of specific neurobiological systems, but are just "better" at dealing with the presented circumstances in their environment. I believe this is where the I-function comes in to counteract genetic predisposition, and to allow the individual to make an informed, or impulsive decision. To some degree, the I-function allows the individual to control their actions, which can account for individuals who have decreased activity in specific neurobiological systems, but not do not exhibit antisocial behavior.

I'm also curious to know as to where society draws the line between individuals who exhibit antisocial behavior, and those who exhibit antisocial tendencies. Antisocial behavior can have different meanings to different people, and its is not farfetched to say that those who may appear to exhibit antisocial tendencies, such as aggressive behavior, are actually behaving in a manner that is heavily influenced by their environment and do have a sense that their behavior is considered "abnormal".

Works Cited
1. Bechara, A., Damasio, H., Damasio, A. R., & Lee, G. P. (1999). Different contributions of the human amygdala and ventromedial prefrontal cortex to decision-making. Journal of Neuroscience, 19, 5473-5481.

2. Fombonne, E., Wostear, G., Cooper, V., Harrington, R., & Rutter, M. (2001). The Maudsley long-term follow-up of child and adolescent depression. I. Psychiatric outcomes in adulthood. British Journal of Psychiatry, 179, 210-217.

3. Moffit, Terrie. Gene may protect abused kids against behavior problems. 1 Aug 2002, EurekAlert, 29 Mar 2009. Normal 0 false false false EN-US X-NONE X-NONE MicrosoftInternetExplorer4

4. Raine, A. (1996). Autonomic nervous system activity and violence. In D. M. Stoff & R. B. Cairns (Eds.), Aggression and violence. Genetic, neurobiological and biological perspectives (pp. 145-168). Mahwah, NJ: Erlbaum.

5. Ronald, Bailey. Born to be Wild? The role of genes in antisocial behavior. 7 Aug 2002. Reason Magazine. 29 Mar 2009. < http://www.reason.com/news/show/34855.html>

6. Van Goozen, S. H. M., Fairchild, G. (2008). How can the study of biological processes help design new interventions for children with severe antisocial behavior?. Development and Psychopathology, 20, 941-973.

7. Zuckerman, M. (1979). Sensation seeking: Beyond the optimum level of arousal. Hillsdale, NJ: Erlbaum.