Abstract:
The molecular events through which social experiences shape future aggressive acts are beginning to be deciphered. The brain serotonin system is by far the major focus of neurobiological inquiries into the mechanisms mediating certain types of aggressive behavior. Its significant role in impulsive, hostile, antisocial and intensely violent outbursts has been supported by several findings including: deficient levels of 5-HT and its acid metabolite; polymorphisms in the genes coding for its metabolic enzymes; mutations in the genes for some of its receptor and transporter molecules; and altered responses to pharmacological challenges of 5-HT agonists. The reciprocal interactions of serotonin with other amines, acids, peptides and steroids provide further evidence that this indolamine mediates impulsive aggressive behavior. Afferent and efferent projections from dopamine and norepinephrine cells to serotonin cells as well as serotonergic presynaptic modulation of catecholaminergic transmission are the basis for serotonin's impact on sensory, integrative motivational and motor facets of aggressive acts. Similarly, serotonin influences the actions of oxytocin and vasopressin as well as corticotrophin releasing factor and opioid peptides in their ultimate effect on aggressive behavior. New tools are required to determine how experience-dependent phasic changes (“state”) in serotonergic terminals in prefrontal cortex, ventral striatum, central and basolateral amygdala, tegmental area and raphé nuclei are superimposed on the serotonin tone in violence-prone individuals (“trait”). Among the urgent research needs are the development of laboratory model systems that capture the transition from the species-typical patterns of dominance or territorial aggression to escalated forms of aggression, since the latter is of primary clinical relevance. The emerging neurobiological research areas focus on: the allosteric modulation of the GABAA receptor and its subunit composition as a site for the escalation of aggressive behavior; the triggering of aggressive acts by glutamate action, presumably via NMDA receptors, in the lateral hypothalamic area; the predisposing role of specific polymorphisms in enzymes and transporter molecules that are critical for the inactivation of monoamines; and the dissociation between catecholaminergic activities in anticipation of intense aggressive encounters vs. the recovery from such interactions. Important targets for intervention are the long-term neuroadaptive changes in DA, opioid peptides and glutamate in the VTA as they are engendered by repeated aggressive experiences, both in the perpetrator and in the victim of aggression.
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The authors express their gratitude to J. Thomas Sopko for his assistance with manuscript preparation and to NIAAA and NIDA grants (AA013983, DA02632) for financial support.
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Miczek, K.A., Faccidomo, S.P., Fish, E.W., DeBold, J.F. (2007). Neurochemistry and Molecular Neurobiology of Aggressive Behavior. In: Lajtha, A., Blaustein, J.D. (eds) Handbook of Neurochemistry and Molecular Neurobiology. Springer, New York, NY. https://doi.org/10.1007/978-0-387-30405-2_7
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