Miczek K.A., DeBold J.F., van Erp A.M.M.
Department of Psychology, Tufts University, 490 Boston Ave, Medford, MA 02155, USA.
Behav Pharmacol. 1994 Aug;5(4 And 5):407-421. doi: 10.1097/00008877-199408000-00004.
Many violent crimes have been associated with alcohol intoxication, but experimental research in laboratory animals has been largely inconclusive on alcohol effects on aggression. A focus on individual differences rather than group statistics has revealed that low doses of ethanol cause large and repeatable increases in aggressive behavior in subgroups of rodents and primates. The recent progress using in vivo neuropharmacological techniques makes it feasible to explore differences in brain mechanisms in animals that show enhanced aggression after ethanol vs those that do not. Effects of ethanol on three major neurotransmitter systems (i.e. GABA, serotonin, dopamine) are examined. Since these neurotransmitter substances are critically important in the neurobiology of various kinds of aggressive behavior in rodent and primate species, they are potential mechanisms by which ethanol alters aggressive behavior. Direct research on the relevance of the physiological interaction between ethanol and the GABA receptor suggests that at least some of the effects of alcohol on aggression involve the GABA(A)-benzodiazepine receptor complex. The role of serotonin (5-HT) will have to be newly defined in light of the findings that ethanol increases 5-HT release in several forebrain areas, in a dose range that can stimulate aggressive behavior in a subgroup of individuals. Recent in vivo studies show that acute exposure to ethanol increases dopamine release in discrete dopamine terminal areas, and that the initiation and execution of aggressive and defensive behavior are also synchronized with increased dopamine activity in these brain regions.
