G C Wagner, H Fisher, N Pole, T Borve, S K Johnson
{"title":"Effects of monoaminergic agonists on alcohol-induced increases in mouse aggression.","authors":"G C Wagner, H Fisher, N Pole, T Borve, S K Johnson","doi":"10.15288/jsas.1993.s11.185","DOIUrl":null,"url":null,"abstract":"<p><p>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.</p>","PeriodicalId":17056,"journal":{"name":"Journal of studies on alcohol. Supplement","volume":"11 ","pages":"185-91"},"PeriodicalIF":0.0000,"publicationDate":"1993-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.15288/jsas.1993.s11.185","citationCount":"16","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of studies on alcohol. Supplement","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.15288/jsas.1993.s11.185","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 16
Abstract
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.