Miczek K A, Altman J L, Appel J B, Boggan W O
Pharmacol Biochem Behav. 1975 May-Jun;3(3):355-61. doi: 10.1016/0091-3057(75)90043-x.
Both p-chlorophenylalanine (PCPA) and PCPA methyl ester were found to reliably induce mouse-killing in non-killer rats only when unusually large doses were used (three successive daily injections of 300 mg/kg) and brain serotonin (5-HT) concentration was drastically reduced (about 90 percent). Neither three doses of 100 mg/kg of PCPA nor p-chloroamphetamine (3 times 3.5 mg/kg) caused similar effects in spite of the fact that these compounds depleted brain 5-HT by 85 percent and 60 percent, respectively. PCPA-induced mouse killing was reversed by 5-HTP (100 mg/kg) only when this serotonin precursor completely restored levels of 5-HT. The topography of PCPA-induced killing did not resemble normal interspecies aggression and was also directed toward fat pups. These findings suggest that 5-HT depletion might facilitate nonspecific killing reactions, but is not a sufficient condition to induce the species-specific predatory behavior in rats.
对氯苯丙氨酸(PCPA)和对氯苯丙氨酸甲酯仅在使用超大剂量(连续三天每日注射300mg/kg)且脑血清素(5-HT)浓度大幅降低(约90%)时,才会可靠地诱导非杀伤性大鼠出现杀鼠行为。尽管100mg/kg的PCPA三次给药和对氯苯丙胺(3次3.5mg/kg)分别使脑5-HT耗竭了85%和60%,但均未产生类似效果。仅当5-羟色氨酸(100mg/kg)使血清素前体完全恢复5-HT水平时,才能逆转PCPA诱导的杀鼠行为。PCPA诱导的杀鼠行为模式与正常种间攻击行为不同,且也针对肥胖幼崽。这些发现表明,5-HT耗竭可能会促进非特异性杀伤反应,但并非诱导大鼠种特异性捕食行为的充分条件。