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苯环利定诱导切碎的纹状体组织释放[3H]多巴胺。

Phencyclidine-induced release of [3H]dopamine from chopped striatal tissue.

作者信息

Ary T E, Komiskey H L

出版信息

Neuropharmacology. 1982 Jul;21(7):639-45. doi: 10.1016/0028-3908(82)90006-5.

Abstract

Phencyclidine was examined for its ability to release [3H]dopamine ([3H]DA) from prelabelled chopped rat striatal tissue. A dynamic perfusion system was used in order to minimize the effects of drugs on uptake mechanisms. Cocaine and S-(+)-amphetamine were used to distinguish uptake inhibition from a neurotransmitter releasing action. Phencyclidine, starting at 3 microM caused a dose-dependent increase in efflux of [3H]DA from chopped striatal tissue. In this same preparation, cocaine, a known neuronal uptake inhibitor of dopamine, was unable to release [3H]DA except in the largest dose of 100 microM. S-(+)Amphetamine, a known releaser of neuronal dopamine, was found to be about ten times more potent then phencyclidine in causing a dose-dependent release of [3H]DA. The results of the above experiments are discussed in relation to the ability of phencyclidine to decrease the synaptosomal accumulation of [3H]DA. It is concluded that some of the psychoactive effects of phencyclidine may be due to the ability of phencyclidine to elicit a release of dopamine from dopaminergic neurons.

摘要

研究了苯环己哌啶从预先标记的大鼠纹状体切碎组织中释放[3H]多巴胺([3H]DA)的能力。使用动态灌注系统以尽量减少药物对摄取机制的影响。可卡因和S-(+)-苯丙胺用于区分摄取抑制和神经递质释放作用。从3 microM开始,苯环己哌啶使切碎的纹状体组织中[3H]DA的流出呈剂量依赖性增加。在同一实验制剂中,可卡因是一种已知的多巴胺神经元摄取抑制剂,除了100 microM的最大剂量外,无法释放[3H]DA。S-(+)苯丙胺是一种已知的神经元多巴胺释放剂,在引起[3H]DA剂量依赖性释放方面,其效力比苯环己哌啶强约十倍。结合苯环己哌啶降低[3H]DA突触体积累的能力,讨论了上述实验结果。得出的结论是,苯环己哌啶的一些精神活性作用可能归因于其从多巴胺能神经元释放多巴胺的能力。

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