Sheard M H, Davis M
Eur J Pharmacol. 1976 Dec;40(2):295-302. doi: 10.1016/0014-2999(76)90066-2.
In a series of experiments the effects of p-chloroamphetamine (PCA) on shock-elicited aggression in rats were investigated. 15 min after 5 mg/kg PCA, shock elicited aggression was inhibited. 2 h to 4 weeks after PCA, fighting was facilitated. Both the inhibitory and the excitatory effects of PCA were directly related to the dose of PCA (1.5, 2.5 OR 5 mg/kg) and were blocked by pretreatment with p-chlorophenylalanine but not by alpha-methyl-p-tyrosine. PCA-increased pain thresholds 15 min after injection and then decreased pain thresholds over the next 24 h but not thereafter, even though shock-elicited aggression continued to be facilitated. The results are consistent with the idea that inhibition of shock-elicited aggression is associated with enhanced release of serotonin whereas enhancement of shock-elicited aggression is associated with serotonin depletion.
在一系列实验中，研究了对氯苯丙胺（PCA）对大鼠电击诱发攻击行为的影响。给予5mg/kg PCA 15分钟后，电击诱发的攻击行为受到抑制。PCA给药后2小时至4周，打斗行为增加。PCA的抑制和兴奋作用均与PCA剂量（1.5、2.5或5mg/kg）直接相关，且可被对氯苯丙氨酸预处理阻断，但不能被α-甲基对酪氨酸阻断。注射PCA 15分钟后疼痛阈值升高，随后在接下来的24小时内疼痛阈值降低，但此后不再降低，尽管电击诱发的攻击行为持续增加。这些结果与以下观点一致：电击诱发攻击行为的抑制与血清素释放增加有关，而电击诱发攻击行为的增强与血清素耗竭有关。
