While no universally accepted definition of aggression exists, the definition suggested by Moyer is one of the most commonly used. Aggression is defined as “overt behavior with the intention of inflicting damage or other unpleasantness upon another individual” (Moyer, 1968). In fact, one cannot imagine modern life without aggression. Everyone is affected by it one way or another. People may be directly engaged in aggression themselves, they can serve as its target, they can be observers of it in others, or control its emergence and growth.
Needless to say, aggression causes considerable problems at different levels, from societal to personal; they range from sensational violence commonly described in the media to everyday episodes affecting everyone. Official statistics shows the increase in crimes caused by aggression. For example, US police reports of criminal acts in 1990 show one violent crime appeared every 17 seconds. If compared to the statistics of 1986, the rates of violence have increased by more than 20 %. In the mid 1990s, FBI statistics shows that the rates are rising at about 9 percent annually. One should keep in mind that this statistics does not include private, non-reported aggression which has, unfortunately, become a part of every day life (Renfrew, 1997, p.3).
To change this drastic situation sufficient knowledge in the field of aggression is required. The current paper is concerned with the biology of aggression, particularly the role of brain in aggression.
Being an outcome of various causes (biological, psychological, social and others) aggression originates from the brain. While there is no sufficient knowledge on the effects of every part of the brain in aggression, two areas of the brain that cause aggression have been defined: the amygdala and the hypothalamus. The amygdala is an area that causes aggression whereas the hypothalamus is a regulator in aggression. The knowledge of brain mechanisms is important for understanding the evolution and dynamics of aggression.
The amygdala is a part of the limbic system that is involved in motivation and emotion. In fact, there are two amygdalae in the human brain: one in each hemisphere, particularly within the temporal lobes (Aggelton, 1968). It releases hormones into the brain when a person receives a stimulus; this causes an emotional reaction which, in its turn, can produce physical reaction.
It is important to note that stimulating the amygdala can cause two opposite reactions and this process depends on the nature of stimulus. Studies with monkeys showed that stimulating the amygdala can cause a docile animal to become aggressive and an aggressive animal to become docile. According to Aronson (1999), when the monkey that is stimulated has access to less dominant monkeys it will become aggressive.
On the other hand, if the monkey under experiment is around more dominant monkeys, it will either put up its defenses or run away (Aronson, 1999, p.270). In each case, as soon as the stimulation to the amygdala is stopped, the abnormal actions of the monkey cease. The study has also shown that if monkey’s aggressive action is already taking place, an electrical charge to the amygdala immediately stops the negative behavior.
This concept of different reactions to a stimulus can be applicable to humans, as well. The classical example is the one where two people are fighting. If one person feels bigger and more dominant than another, he or she will apt to attack. Meanwhile, if the latter person feels less dominant than the former, then he or she will either put up a fight or go away. In the case when both people feel equally dominant the fight will go on. The fight can be avoided if the participants feel they are less dominant, hence, they will not feel the power to engage into the fight.
The role played by amygdala in failing to regulate aggression is demonstrated by the following case. In August, 1966, 25-year old student of the University of Texas, Charles Whitman, killed 14 people from the top floor of the school’s observatory tower with a high-powered rifle. Actually, he proceeded to shoot at 31 people, 14 of them were killed. Also, police discovered the bodies of Whitman’s wife and mother in their homes. In the notes that the killer left he mentioned that he had been experiencing “unusual and irrational thoughts” and wondered if his rage could be explained by some sort of physical abnormality. Whitman turned to be right – there was a walnut-sized tumor found pressing into his amygdala. The cancerous growth caused his abnormal behavior (BlogMeister, 2007).
A thorough examination of the human brain anatomy and its physiology can help experts foresee aggressive behavior or impulse control disorders in preschool aged children. For instance, in a study presented in November 2007 at the Society for Neuroscience conference in San Diego, scientists have studied brain activity in a small group of boys that were considered “reactively aggressive” wherein, according to their definition, means that they used to punch others or break something but afterwards they felt sorry about it (Singer, 2007). Boys who could control their behavior also took part in the experiment.
The subjects were shown the images of threatening faces, those who failed to control themselves had greater activity in the amygdala compared to those who could control their behavior. The study showed that the reactively aggressive boys feel more fearful when they look at angry faces, and it reflects in the increased activity in the amygdala.
Further studies, conducted by Raine and his colleagues have shown that the prefrontal cortices of murderers and people with antisocial behavior were smaller than those of controls. Moreover, all those people had both structural and functional impairments in their prefrontal cortices (Goode, 2000).
As aggression is significant in terms of social regulation and social interaction, it involves the cortex of the frontal lobes of the brain. Since the frontal cortex is associated with the amygdala and the hypothalamus, the frontal cortex influences these brain centers that control aggression. A damaged frontal lobe causes overt behavior in humans. Patients with this problem react impulsively, do not plan beforehand their behavior and do not foresee its consequences. They tend to have short tempers, always respond to minor provocation and cannot control their emotions (Anderson et al., 1999, pp.1032-1037).
The hypothalamus is another part of brain that plays a significant role in aggression. It is located below the thalamus, just above the brain step and links the nervous system to the endocrine system via hypophysis. The hypothalamus is believed to be a regulator in aggression. The experiments have shown that hypothalamus causes aggressive behavior when electrically stimulated (Hermans et al, 1983). For instance, in a study by Hermans et al (1983), over 400 sites in the hypothalami of 270 male rats were electrically stimulated with the purpose to call fights between the rats. As a result, the localization of the electrodes that induce fights differed from the localization of electrodes where no fights were induced.
A non-parametric discriminant analysis was used to detect and test the differences in localization of the electrodes. The procedure allowed delimiting areas within the hypothalamus with different probability to induce aggression. In addition, the experiment helped to discriminate between the lowest thresholds for attack behavior and those where the fiercest forms of attack behavior are induced (Hermans et al., 1983). Moreover, the research showed that the hypothalamus has receptors that help to determine the levels of aggression depending on these receptors’ interactions with neurotransmitters such as serotonin and vasopressin.
Changes in the level and metabolism of serotonin impact affective behavior in general and aggressive behavior, in particular. The studies of suicidal and impulsive aggressive behavior in humans focus on the role of serotonin since there is a correlation between low serotonin concentration in the brain and aggressive behavior. Manipulation with serotonergic system influences aggressive behaviors. Namely, depletion of brain serotonin increases aggression and enhancing of brain serotonin reduces aggression. Actually, there exists a class of drugs acting on serotonin, these serotonergic-enhancing drugs, known as “serenics” reduce aggression (Olivier, 2000, pp. 207-217).
As far as vasopressin and serotonin are concerned, one more research acquires special significance:
Studies in several species of rodents show that arginine vasopressin (AVP) acting through a V1A receptor facilitates offensive aggression, i.e., the initiation of attacks and bites, whereas serotonin (5-HT) acting through a 5-HT1B receptor inhibits aggressive responding. One area of the CNS that seems critical for the organization of aggressive behavior is the basolateral hypothalamus, particularly the anterior hypothalamic region. The present studies examine the neuroanatomical and neurochemical interaction between AVP and 5-HT at the level of the anterior hypothalamus (AH) in the control of offensive aggression in Syrian golden hamsters.
First, specific V1A and 5-HT1B binding sites in the AH are shown by in vitro receptor autoradiography. The binding for each neurotransmitter colocalizes with a dense field of immunoreactive AVP and 5-HT fibers and putative terminals. Putative 5-HT synapses on AVP neurons in the area of the AH are identified by double-staining immunocytochemistry and laser scanning confocal microscopy. These morphological data predispose a functional interaction between AVP and 5-HT at the level of the AH. When tested for offensive aggression in a resident/intruder paradigm, resident hamsters treated with fluoxetine, a selective 5-HT reuptake inhibitor, have significantly longer latencies to bite and bite fewer times than vehicle-treated controls.
Conversely, AVP microinjections into the AH significantly shorten the latency to bite and increase biting attacks. The action of microinjected AVP to increase offensive aggression is blocked by the pretreatment of hamsters with fluoxetine. These data suggest that 5-HT inhibits fighting, in part, by antagonizing the aggression-promoting action of the AVP system (Delville et al, 1997).
Brain dopamine is another neurochemical implicated in aggression. According to numerous animal studies increasing brain activity creates a state in which animals are inclined to respond aggressively to stimuli in the environment. Therefore, management of violent patients is impossible without resorting to therapeutic agents like antagonists of dopamine receptors. We should also admit the fact that dopamine has important role in reward and punishment that is considered to be the real reason why dopamine contributes to the display of aggression.
Further, noradrenaline correlates with aggressive behavior. Medicine has studied this correlation and has found noradrenergic receptor blockade extremely useful in treatment of violent patients.
Apart from vasopressin, many other peptides, that act as neurotransmitters are found in the brain. Though alternations in several of them are known to change aggression, there is no single one that is specifically associated with it. Thus, current studies of aggression should investigate the existence of such components. Further research in the field under consideration should continue to throw light on the role of brain in aggression.
Though the existing knowledge enables us to say that aggression originates from the brain, there is a need to continue the research in this area. A thorough understanding of the link between the brain and aggression will contribute to the general understanding of the complexity of aggression which, in turn, would lead to direct help to those who try to control it in either animals or humans.
References
Aggleton, P. (1968). The amygdala. Wiley-Liss. Amygdala. Web.
Anderson W. et al. (1999). A damaged frontal lobe causes overt behavior in humans [Electronic version]. Nature Neuroscience 2, 1032 – 1037.
Aronson , E. (1999). The social animal (8th ed.). New York: Worth Publishers.
BlogMeister. (2007). Amygdala abnormalities linked to violent aggression. Web.
Delville, Y. et al. (1997). Vasopressin/Serotonin Interactions in the Anterior Hypothalamus Control Aggressive Behavior in Golden Hamsters. Web.
Goode, E. (2000). Study of 21 men with antisocial disorder finds less gray matter [Electronic version]. New York Times, A-4.
Hermans, J. et al. (1983). Discriminant Analysis of the Localization of Aggression-Inducing Electrode Placements in the Hypothalamus of Male Rats. Web.
Moyer, K.E. (1968). Kinds of aggression and their physiological basis. Communications in Behavioural Biology, 2-A: 65-87.
Olivier, B., Oorschot, R. (2000). 5-HT1B receptors and aggression. European Journal of Pharmacology, 526, 207-217.
Renfrew, J. W. (1997). Aggression and Its Causes: A Biopsychosocial Approach. New York: Oxford University Press.
Singer, E. (2007). The Neurological Roots of Aggression. Web.