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调控口面运动:氨基酸机制与突变模型。

Regulation of orofacial movement: amino acid mechanisms and mutant models.

机构信息

Advanced Research Institute for the Sciences and Humanities, Nihon University, Tokyo 102, Japan.

出版信息

Int Rev Neurobiol. 2011;97:61-75. doi: 10.1016/B978-0-12-385198-7.00003-5.

Abstract

Generation and regulation of orofacial movements involve complex mechanisms that include primary roles not only for dopamine but also the amino acid neurotransmitters γ-aminobutyric acid (GABA) and glutamate. However, the roles of individual GABA and glutamate receptor subtypes, subunits and associated processes are unclear. Here we outline studies of motor function in mutant mice with "knockout" of GABA and glutamate receptor subtypes. We then review systematic studies of orofacial movements in mutants with (i) "Knockout" of phospholipase C-related catalytically inactive protein (PRIP), which regulates cell surface expression of GABA(A) receptors containing a γ2 subunit, and: (ii) Heterozygous deletion of neuregulin-1 which, inter alia, regulates glutamate receptor-mediated processes. Each of GABAergic and glutamatergic sytems regulate specific topographies of orofacial movement both individually and via interactions with dopaminergic processes.

摘要

口面部运动的产生和调节涉及复杂的机制,不仅包括多巴胺的主要作用,还包括氨基酸神经递质γ-氨基丁酸(GABA)和谷氨酸。然而,个别 GABA 和谷氨酸受体亚型、亚基和相关过程的作用尚不清楚。在这里,我们概述了对具有 GABA 和谷氨酸受体亚型“敲除”的突变小鼠运动功能的研究。然后,我们回顾了对具有以下特征的突变体的口面部运动进行的系统研究:(i)“敲除”磷脂酶 C 相关无催化活性蛋白(PRIP),该蛋白调节含有γ2 亚基的 GABA(A)受体的细胞表面表达,以及:(ii)神经调节素-1 的杂合缺失,其除其他外,调节谷氨酸受体介导的过程。GABA 能和谷氨酸能系统都通过与多巴胺能过程的相互作用,单独和相互调节口面部运动的特定拓扑结构。

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