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右旋苯丙胺和可卡因对灵长类动物社会行为的破坏:抗精神病药物的差异拮抗作用。

Disruption of primate social behavior by d-amphetamine and cocaine: differential antagonism by antipsychotics.

作者信息

Miczek K A, Yoshimura H

出版信息

Psychopharmacology (Berl). 1982;76(2):163-71. doi: 10.1007/BF00435272.

Abstract

Psychostimulants lead to withdrawal from social interactions and to a decline of affective behavior in squirrel monkeys. These changes, in addition to motor stereotypies, may be related to stimulant-induced psychosis in humans. In the first of two series of experiments, 1 mg/kg d-amphetamine or 10 mg/kg cocaine, administered orally three times over 24 h to one adult male member of an established group (n = 6-9), engendered stereotyped movements of the head and hands, reduced rest postures, and greatly reduced all forms of social initiatives. Chlorpromazine (0.25-1.0 mg/kg), haloperidol (0.25, 0.5 mg/kg), and physostigmine (0.04, 0.08 mg/kg), administered before the third amphetamine or cocaine injection, blocked the motor stereotypies and hyperactivity. Chlorpromazine, haloperidol, and physostigmine did not reliably antagonize the pronounced reduction in social behavior. The second series of experiments focused on agonistic behavior in the context of resident-intruder confrontations and on affiliative behavior toward group members. d-Amphetamine (3 X 0.5 mg/kg) and, to a lesser extent, cocaine (3 X 10 mg/kg) decreased affiliative and agonistic behavior. Chlorpromazine (0.5, 1.0 mg/kg) and haloperidol (0.1, 0.25 mg/kg) did not block the severe disruption of the affiliative and agonistic behavior in amphetamine-treated monkeys; physostigmine (0.06 mg/kg) reversed the decline in time spent close to the familiar monkey in amphetamine-treated monkeys. By contrast, stimulant-induced stereotypies were effectively antagonized by chlorpromazine, haloperidol, and physostigmine. These results suggest that psychostimulant-induced changes in primate social behavior may be mediated by mechanisms other than those underlying motor stereotypies.

摘要

精神兴奋剂会导致松鼠猴退出社交互动,并使其情感行为出现衰退。除了运动刻板行为外,这些变化可能与人类中兴奋剂诱发的精神病有关。在两组实验的第一组中,对一个已组建群体中的一只成年雄性成员(n = 6 - 9)在24小时内分三次口服给予1毫克/千克的右旋苯丙胺或10毫克/千克的可卡因,引发了头部和手部的刻板动作、休息姿势减少以及各种社交主动性行为大幅减少。在第三次注射苯丙胺或可卡因之前给予氯丙嗪(0.25 - 1.0毫克/千克)、氟哌啶醇(0.25、0.5毫克/千克)和毒扁豆碱(0.04、0.08毫克/千克),可阻断运动刻板行为和多动。氯丙嗪、氟哌啶醇和毒扁豆碱并不能可靠地对抗社交行为的显著减少。第二组实验聚焦于领地 - 入侵者对抗情境下的攻击行为以及对群体成员的亲和行为。右旋苯丙胺(3×0.5毫克/千克)以及在较小程度上可卡因(3×10毫克/千克)会减少亲和行为和攻击行为。氯丙嗪(0.5、1.0毫克/千克)和氟哌啶醇(0.1、0.25毫克/千克)并不能阻断苯丙胺处理的猴子中亲和行为和攻击行为的严重破坏;毒扁豆碱(0.06毫克/千克)可逆转苯丙胺处理的猴子中靠近熟悉猴子的时间减少的情况。相比之下,氯丙嗪、氟哌啶醇和毒扁豆碱可有效对抗兴奋剂诱发的刻板行为。这些结果表明,精神兴奋剂诱发的灵长类动物社交行为变化可能由运动刻板行为背后的机制以外的其他机制介导。

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