Accumbal dopamine and serotonin in anticipation of the next aggressive episode in rats.

Autonomic and limbic neural activities are linked to aggressive behavior, and it is hypothesized that activities in the cardiovascular and monoaminergic systems play a role in preparing for an aggressive challenge. The objective was to learn about the emergence of monoamine activity in nucleus accumbens before an aggressive confrontation that was omitted at the regular time of occurrence, dissociating the motoric from the aminergic activity. Dopamine, serotonin, heart rate and behavioral activity were monitored before, during and after a single 10-min confrontation in resident male Long-Evans rats fitted with a microdialysis probe in the n. accumbens and with a telemetry sender (experiment 1). DA, but not 5-HT efflux, was confirmed to increase in n. accumbens during and after a single aggressive episode. In aggressive males that confronted an opponent daily for 10 days (experiment 2) heart rate rose 1 h before the regularly scheduled encounter relative to control rats, as measured on day 11 in the absence of any aggression. Concurrently, DA levels increased by 60-70% over baseline levels and 5-HT levels decreased by 30-35% compared to baseline levels. These changes were sustained over 1 h, and contrasted with no significant changes in DA, 5-HT, heart rate or behavioral activity in control rats. The rise in mesolimbic DA appears to be significant in anticipating the physiological and behavioral demands of an aggressive episode, and the fall in 5-HT in its termination, dissociated from the actual execution of the behavior.

Neuropharmacological characteristics of individual differences in alcohol effects on aggression in rodents and primates.

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.