University of London, School of Pharmacy, Department of Pharmacology 29/39 Brunswick Square, London WC1N 1AX, UK.
Curr Neuropharmacol. 2009 Jun;7(2):125-31. doi: 10.2174/157015909788848875.
Several lines of evidence suggest that the modulation of presynaptic GABA release is mediated by a variety of receptors including; presynaptic AMPA, cannabinoid, GABA(B), kainate, metabotropic glutamate, NMDA, and opioid receptors. The evidence supporting presynaptic modulation of inhibition is predominantly obtained from studying stimulus elicited, spontaneous or miniature synaptic events, where the information regarding the identity of the presynaptic cell is lost. This article summarises these findings then focuses on another approach to study the presynaptic modulation of GABA release by comparing the modulation of GABA release at unitary synapses identified morphologically, immunocytochemically and electrophysiologically. To date, evidence for cell-type specific regulation of presynaptic inhibition at identified synapses involving most of the above presynaptic receptors does not exist. Therefore, the key presynaptic modulators that will be focused on here are kainate and cannabinoid receptors and their intracellular signalling cascades that orchestrate GABA release. There will be some discussion on presynaptic modulation via opioid receptors at identified synapses. This review provides evidence to suggest a cell-type specific modulation of presynaptic inhibition in cortical regions.
有几条证据表明，前突触 GABA 释放的调制是由多种受体介导的，包括：前突触 AMPA、大麻素、GABA(B)、 kainate、代谢型谷氨酸、NMDA 和阿片受体。支持抑制性前突触调制的证据主要来自于研究刺激诱发的、自发的或微小的突触事件，其中关于前突触细胞身份的信息丢失了。本文总结了这些发现，然后通过比较形态学、免疫细胞化学和电生理学上鉴定的单位突触 GABA 释放的调制，重点关注另一种研究 GABA 释放的前突触调制的方法。迄今为止，涉及上述大多数前突触受体的、在已鉴定的突触中针对前突触抑制的细胞类型特异性调节的证据尚不存在。因此，这里将重点关注 kainate 和大麻素受体及其细胞内信号级联，它们协调 GABA 的释放。本文将对已鉴定的突触中通过阿片受体的前突触调制进行一些讨论。本综述提供的证据表明，皮质区域的前突触抑制存在细胞类型特异性调节。
