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[非典型抗精神病药物卡比定和舒必利对大鼠伏隔核突触体中多巴胺生物合成的影响]

[Effect of the atypical neuroleptics carbidine and sulpiride on dopamine biosynthesis in the synaptosomes of the nucleus accumbens septi in rats].

作者信息

Kudrin V S, Hetey L, Morgenshtern R, Raevskiĭ K S, Olssner W

出版信息

Farmakol Toksikol. 1987 Mar-Apr;50(2):16-20.

PMID:2884129
Abstract

Neurochemical mechanisms of actions of atypical neuroleptics carbidine (a derivative of gamma-carboline) and sulpiride on dopamine (DA) biosynthesis in synaptosomes of the nucleus accumbens septi of the rat brain were studied. Carbidine caused a dose-dependent decrease of the animals' locomotor hyperactivity induced by apomorphine (1 mg/kg). Both carbidine and sulpiride administered in a dose of 5 mg/kg increased the activity of tyrosine hydroxylase in synaptosomes of the nucleus accumbens septi. In vitro carbidine decreased and sulpiride exerted no effect on the activity of tyrosine hydroxylase of the nucleus accumbens septi synaptosomes. Carbidine as well as sulpiride in vitro failed to modify the release of 3H-DA from superfused synaptosomes. At the same time, both in vivo and in vitro, the two neuroleptics reduced the inhibitory effect of DA on the 3H-DA release from synaptosomes of the nucleus accumbens septi and on the activity of tyrosine hydroxylase.

摘要

研究了非典型抗精神病药物卡比定(一种γ-咔啉衍生物)和舒必利对大鼠脑伏隔核突触体中多巴胺(DA)生物合成的神经化学作用机制。卡比定可使阿扑吗啡(1毫克/千克)诱导的动物运动性多动呈剂量依赖性降低。卡比定和舒必利均以5毫克/千克的剂量给药时,可增加伏隔核突触体中酪氨酸羟化酶的活性。在体外,卡比定可降低伏隔核突触体酪氨酸羟化酶的活性,而舒必利则无此作用。卡比定和舒必利在体外均未能改变超融合突触体中3H-DA的释放。同时,在体内和体外,这两种抗精神病药物均降低了DA对伏隔核突触体中3H-DA释放和酪氨酸羟化酶活性的抑制作用。

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