Nicotinic acetylcholine receptor subtypes involved in facilitation of GABAergic inhibition in mouse superficial superior colliculus
Nicotinic acetylcholine receptor subtypes involved in facilitation of GABAergic inhibition in mouse superficial superior colliculus
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DOI：
10.1152/jn.00211.2005
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发表时间：
2005-12-01
影响因子：
2.5
通讯作者：
Isa, T
中科院分区：
文献类型：
--
作者：
Endo, T;Yanagawa, Y;Isa, T
浅上丘（sSC）是与视觉显着性相关的感觉处理中的关键站。 sSC 接收来自副二联核的胆碱能投射，之前的研究表明 sSC 中存在几种不同的烟碱乙酰胆碱受体 (nAChR) 亚基。在这项研究中，为了阐明胆碱能输入对 sSC 的作用，我们使用从谷氨酸脱羧酶 67-绿色荧光蛋白 (GFP) 敲入小鼠获得的体外切片制剂检查了 ACh 在 GABA 能和非 GABA 能 sSC 神经元中诱导的电流反应，其中 GFP 在 GABA 能神经元中特异性表达。短暂施加乙酰胆碱 (ACh) 气压会在 GABA 能和非 GABA 能神经元中引发烟碱内向电流反应。 GABA 能神经元的内向电流反应对含有 α 3 β 2 和 α 6 β 2 受体的选择性拮抗剂 α-芋螺毒素 MII (α CtxMII) 高度敏感。这些神经元的一个子集表现出更快的 α-金环蛇毒素敏感内向电流分量，表明含有 α7 的 nAChR 的表达。我们还发现突触前 nAChR 的激活诱导 GABA 的释放，从而在非 GABA 能神经元中引发由 GABA(A) 受体介导的微型抑制性突触后电流的爆发。这种 ACh 诱导的 GABA 释放主要由 α CtxMII 敏感的 nAChR 介导，是电压依赖性钙通道激活的结果。形态学分析显示，记录的 GFP 阳性神经元为中间神经元，GFP 阴性神经元包括投射神经元。这些发现表明 nAChR 参与 GABA 能抑制的调节并调节 sSC 的视觉处理。
The superficial superior colliculus (sSC) is a key station in the sensory processing related to visual salience. The sSC receives cholinergic projections from the parabigeminal nucleus, and previous studies have revealed the presence of several different nicotinic acetylcholine receptor (nAChR) subunits in the sSC. In this study, to clarify the role of the cholinergic inputs to the sSC, we examined current responses induced by ACh in GABAergic and non-GABAergic sSC neurons using in vitro slice preparations obtained from glutamate decarboxylase 67-green fluorescent protein (GFP) knock-in mice in which GFP is specifically expressed in GABAergic neurons. Brief air pressure application of acetylcholine (ACh) elicited nicotinic inward current responses in both GABAergic and non-GABAergic neurons. The inward current responses in the GABAergic neurons were highly sensitive to a selective antagonist for alpha 3 beta 2- and alpha 6 beta 2-containing receptors, alpha-conotoxin MII (alpha CtxMII). A subset of these neurons exhibited a faster alpha-bungarotoxin-sensitive inward current component, indicating the expression of alpha 7-containing nAChRs. We also found that the activation of presynaptic nAChRs induced release of GABA, which elicited a burst of miniature inhibitory postsynaptic currents mediated by GABA(A) receptors in non-GABAergic neurons. This ACh-induced GABA release was mediated mainly by alpha CtxMII-sensitive nAChRs and resulted from the activation of voltage-dependent calcium channels. Morphological analysis revealed that recorded GFP-positive neurons are interneurons and GFP-negative neurons include projection neurons. These findings suggest that nAChRs are involved in the regulation of GABAergic inhibition and modulate visual processing in the sSC.