Identification of disruptions in brain areas linked to impulsive aggressive behavior and making ethical judgments may give deeper insight into the neurobiology of violence. Aggressive encounters increase vulnerability to depression and immune illnesses by changing the brains of both aggressors and their victims.
In one study, the brain images of 792 antisocial persons were compared to images of 704 control subjects. The first tended to have damage in brain structures involved in making moral judgments like the dorsal and ventral prefrontal cortex, the amygdala, and the angular gyrus. A hyperactive response in the amygdala, which processes data on threats and fear, together with a lesser activity in the frontal lobe that is responsible for decision-making and impulse control was identified in teenage boys with inadequately high aggression toward perceived threats. Reactive-affective-defensive-impulsive (RADI) behavior describes defensive aggressive impulses and results from such disproportionate fear and diminished self control.
Low concentrations of serotonin in the cerebral spine serve as a marker and predictor of aggressive behavior. Its deficiency might be related to pathological violence, which if unchecked can change the brain to cause serotonin decrease. Transition from adaptive aggressive behavior into abnormal forms that inflict harm can be due to not structural but functional changes in certain serotonin receptors.
A neurotransmitter arginine-vasopressin (AVP) released in the amygdala helps regulate maternal aggression. When synthesized in the brain and released to the kidneys, it helps regulate the water retention. AVP plays a role in male aggression and pair-bonding. Blocking its receptors results in lower anxiety and agression, and synthetic AVP makes animals more anxious and aggressive. Oxytocin, a neurotransmitter released during birth and breastfeeding, reduces anxiety and fear, which might enable more aggressive reaction to possible threats.
Aggression damages the victim but has negative repercussions also for the aggressor. Marker of stress, corticosterone levels, are significantly increased soon after and remain elevated. Some cytokines, the molecules within the immune system that signal the presence of pathogens, also are elevated in the prefrontal cortex for both. Aggressive interactions cause both dominant and submissive mice to become hyperactive. Motor activity remains high in dominant individuals and declines in the submissive ones. Brain levels in the hippocampus of the neurotransmitter noradrenaline, which can help mediate the effects of stress, fall in of the dominant mice. However, in the central amygdala it increases in submissive mice.
Stressful encounters has a profound influence on the neuroendocrine and neurochemical systems. They cause chemical changes in many areas of the brain, including those involved in emotions: the prefrontal cortex, the hippocampus, and the amygdala. Some of the neurotransmitters and hormones impacted by stress are dopamine, serotonin, noradrenalin, and corticotropin-releasing hormone (CRH).
