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对氯苯丙氨酸对大鼠休克诱导的攻击和按压反应的影响。

p-Chlorophenylalanine effects on shock-induced attack and pressing responses in rats.

作者信息

Sewell R G, Gallus J A, Gault F P, Cleary J P

出版信息

Pharmacol Biochem Behav. 1982 Nov;17(5):945-50. doi: 10.1016/0091-3057(82)90477-4.

Abstract

The literature concerning the effects of d,1-parachlorophenylalanine (PCPA) upon shock-induced aggression (SIA) was examined and found to be inconsistent. PCPA, a known serotonin depletor, has behavioral effects in a variety of other procedures which collectively suggest that PCPA should produce SIA enhancement. The present study analyzed PCPA (300 mg/kg, IP) effects upon SIA in rats restrained spatially close to an inanimate target and panel operandum. The results showed marked increases in both aggressive biting and panel-pressing for several days following each PCPA treatment, for each subject tested. These data were interpreted to indicate that serotonin depletion by PCPA does indeed enhance SIA but that this effect is not selective for aggression. Potential controlling variables are suggested to account for reports of no effect on SIA after PCPA treatment. It is concluded that procedural variables may be the critical determinants of variation in reported PCPA-aggression effects across studies, rather that hypothesized differences in neurochemical mediators.

摘要

对有关消旋对氯苯丙氨酸(PCPA)对休克诱导攻击行为(SIA)影响的文献进行了研究,发现结果并不一致。PCPA是一种已知的血清素消耗剂,在各种其他实验程序中具有行为效应,这些效应共同表明PCPA应该会增强SIA。本研究分析了PCPA(300mg/kg,腹腔注射)对空间上靠近无生命目标和面板操作部件的大鼠SIA的影响。结果显示,在每次对每个受试对象进行PCPA处理后的几天里,攻击咬人和按压面板行为均显著增加。这些数据被解释为表明PCPA导致的血清素耗竭确实增强了SIA,但这种效应并非对攻击行为具有选择性。文中提出了潜在的控制变量,以解释PCPA处理后对SIA无影响的报告。研究得出结论,程序变量可能是各研究中报道的PCPA攻击效应差异的关键决定因素,而非神经化学介质的假设差异。

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