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苯环己哌啶(PCP)和西格玛受体激动剂对γ-氨基丁酸(GABA)诱导的抑制作用的促进是通过儿茶酚胺能途径介导的。

Facilitation of GABA-induced depression with PCP and sigma receptor agonists was mediated through catecholaminergic pathways.

作者信息

Wang Y, Kao M C, Lee H K

机构信息

Department of Pharmacology, National Defense Medical Center, Taipei, Taiwan, Republic of China.

出版信息

Life Sci. 1990;47(22):PL121-6. doi: 10.1016/0024-3205(90)90444-v.

Abstract

The purpose of this experiment was to investigate the interactions of norepinephrine with PCP (phencyclidine) and sigma receptor agonists--modulated GABA (gamma aminobutyric acid) response in the cerebellum. Drugs were directly applied to a single cerebellar Purkinje neuron of urethane-anesthesitized rat through a multibarrel pipette. (+)PCMP [1-(-1-phenylcyclohexyl)-3-methyl piperidine], a PCP receptor agonist, and dexoxadrol, a sigma receptor agonist, significantly enhanced GABA induced inhibition. In norepinephrine-depleted animals, however, both (+)PCMP and dexoxadrol did not modulate GABA's effect. In conclusion, our findings indicated that the PCP/sigma-induced facilitation of GABA reactions were mediated through noradrenergic system in the cerebellum.

摘要

本实验的目的是研究去甲肾上腺素与苯环己哌啶(PCP)和σ受体激动剂在小脑调制γ-氨基丁酸(GABA)反应中的相互作用。通过多管移液管将药物直接施加于经乌拉坦麻醉的大鼠的单个小脑浦肯野神经元上。PCP受体激动剂(+)PCMP [1-(-1-苯基环己基)-3-甲基哌啶]和σ受体激动剂右吗拉胺可显著增强GABA诱导的抑制作用。然而,在去甲肾上腺素耗竭的动物中,(+)PCMP和右吗拉胺均未调节GABA的作用。总之,我们的研究结果表明,PCP/σ诱导的GABA反应促进作用是通过小脑中的去甲肾上腺素能系统介导的。

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