NEUROPHARMACOLOGICAL CHARACTERISTICS OF INDIVIDUAL-DIFFERENCES IN ALCOHOL EFFECTS ON AGGRESSION IN RODENTS AND PRIMATES

Many violent crimes have been associated with alcohol intoxication, bu t experimental research in laboratory animals has been largely inconcl usive on alcohol effects on aggression. A focus on individual differen ces rather than group statistics has revealed that low doses of ethano l cause large and repeatable increases in aggressive behavior in subgr oups of rodents and primates. The recent progress using in vivo neurop harmacological techniques makes it feasible to explore differences in brain mechanisms in animals that show enhanced aggression after ethano l vs those that do not. Effects of ethanol on three major neurotransmi tter systems (i.e. GABA, serotonin, dopamine) are examined. Since thes e neurotransmitter substances are critically important in the neurobio logy of various kinds of aggressive behavior in rodent and primate spe cies, they are potential mechanisms by which ethanol alters aggressive behavior. Direct research on the relevance of the physiological inter action between ethanol and the GABA receptor suggests that at least so me of the effects of alcohol on aggression involve the GABA(A)-benzodi azepine receptor complex. The role of serotonin (5-HT) will have to be newly defined in light of the findings that ethanol increases 5-HT re lease in several forebrain areas, in a dose range that can stimulate a ggressive behavior in a subgroup of individuals. Recent irt vivo studi es show that acute exposure to ethanol increases dopamine release in d iscrete dopamine terminal areas, and that the initiation and execution of aggressive and defensive behavior are also synchronized with incre ased dopamine activity in these brain regions.