Ka. Miczek et al., NEUROPHARMACOLOGICAL CHARACTERISTICS OF INDIVIDUAL-DIFFERENCES IN ALCOHOL EFFECTS ON AGGRESSION IN RODENTS AND PRIMATES, Behavioural pharmacology, 5(4-5), 1994, pp. 407-421
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.