Effects of monoaminergic agonists on alcohol-induced increases in mouse aggression.

Two sets of studies were conducted on alcohol-induced increases in aggression. In the first, the effects of alcohol on target biting and resident-intruder attack were assessed in mice fed a standard diet or one supplemented with 0.5% L-tryptophan. Mice attacked an inanimate target at a high rate following tail shock, an intermediate rate during the intershock interval and a low rate during a tone that preceded the shock. Alcohol increased target biting following shock and during the intershock interval, an effect partially blocked by tryptophan. Resident mice attacked intruders 27.2 +/- 5.3 times per 10-minute session with an average latency of 155 +/- 42 seconds. Alcohol increased the number of attacks and lowered the latency to the first attack. Again, tryptophan partially blocked these effects. Finally, in a second set of mice, the same tryptophan diet was found to potentiate the aggression-reducing effects of fluoxetine and fenfluramine without disrupting motor performance. In the second study, the effects of alcohol administered alone or in combination with tyramine were assessed in the resident-intruder paradigm. Again, it was observed that low doses of alcohol increased the resident attack of intruders. Although this effect was heightened by the co-administration of tyramine, the effect failed to reach statistical significance. These observations are discussed in reference to alcohol-induced increases in offensive and defensive aggression and the possible modulation of this effect by brain monoamines.