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大麻素激动剂对大鼠黑质网状部神经元GABA能输入的突触前抑制作用

Presynaptic inhibition of GABAergic inputs to rat substantia nigra pars reticulata neurones by a cannabinoid agonist.

作者信息

Chan P K, Chan S C, Yung W H

机构信息

Department of Physiology, Faculty of Medicine, The Chinese University of Hong Kong, Shatin.

出版信息

Neuroreport. 1998 Mar 9;9(4):671-5. doi: 10.1097/00001756-199803090-00020.

DOI:10.1097/00001756-199803090-00020
PMID:9559936
Abstract

Whole-cell patch-clamp recordings were made from substantia nigra pars reticulata (SNR) neurones in rat midbrain slices to investigate the electrophysiological effects of cannabinoids. The cannabinoid receptor agonist WIN 55212-2 (10 microM) significantly reduced intranigrally evoked and spontaneous inhibitory post-synaptic currents (IPSCs) which were mediated by GABA(A) receptors. The postsynaptic current induced by bath application of GABA was not affected by the presence of WIN 55212-2. The actions of WIN 55212-2 were not mimicked by the inactive enantiomer WIN 55212-3. WIN 55212-2 also hyperpolarized the membrane of SNR neurones in a tetrodotoxin/0-Ca2+-insensitive manner. These data suggest that cannabinoids modulate the activity of SNR neurones by presynaptic inhibition of GABA inputs. They may also exert a direct post-synaptic inhibition on these neurones.

摘要

采用全细胞膜片钳记录技术,对大鼠中脑切片黑质网状部(SNR)神经元进行记录,以研究大麻素的电生理效应。大麻素受体激动剂WIN 55212-2(10微摩尔)显著降低了由GABA(A)受体介导的黑质内诱发的和自发的抑制性突触后电流(IPSCs)。通过浴灌应用GABA诱导的突触后电流不受WIN 55212-2存在的影响。WIN 55212-2的作用不能被无活性对映体WIN 55212-3模拟。WIN 55212-2还以河豚毒素/零钙不敏感的方式使SNR神经元的膜超极化。这些数据表明,大麻素通过对GABA输入的突触前抑制来调节SNR神经元的活动。它们也可能对这些神经元施加直接的突触后抑制作用。

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