Biochemical correlates in mouse-killing behavior of the rat: prolonged isolation and brain cholinergic function.
After 30 days of isolation, 45% of the rats exhibited mouse-killing behavior. The killing response was suppressed by atropine (5 mg/kg and 8 mg/kg, IP) and scopolamine (8 mg/kg, IP), whereas methylatropine was ineffective. Acetylcholine (ACh) content and acetylcholinesterase (AChE) activity were measured in 5 discrete areas of rat brain. As compared with the aggregated rats only the killer rats exhibited higher ACh levels in the diencephalon. The activity of AChE in all brain areas was unchanged by isolation; no significant difference was found between the killer and nonkiller rats. These results suggest that central cholinergic mechanisms participate in the mediation of mouse-killing behavior in the rat.
D000109:Acetylcholine / Q000378:metabolism*; D000374:Aggression; D000378:Agonistic Behavior / Q000187:drug effects; D000679:Amygdala / Q000378:metabolism; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D001286:Atropine Derivatives; D001921:Brain / Q000378:metabolism*; D001933:Brain Stem / Q000378:metabolism; D002540:Cerebral Cortex / Q000378:metabolism; D003342:Corpus Striatum / Q000378:metabolism; D004027:Diencephalon / Q000378:metabolism; D006801:Humans; D008297:Male; D051381:Rats; D012601:Scopolamine / Q000494:pharmacology; D012934:Social Isolation
D001286:Atropine Derivatives; D001285:Atropine; D012601:Scopolamine; D000109:Acetylcholine