Potassium channels underlie postsynaptic but not presynaptic GABA_B receptor-mediated inhibition on ventrolateral periaqueductal gray neurons

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• 作者：Zhi-Liang Liu^a ; Hongyu Ma^b ; ^{hma005@gmail.com} ; Ru-Xiang Xu^a ; Yi-Wu Dai^a ; Hong-Tian Zhang^a ; Xue-Qin Yao^a ; Kun Yang^c ; ^d ; ^{kyang001@umaryland.edu}
• 关键词：aCSF ; artificial cerebrospinal fluid ; AMPA ; 伪-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid ; AP-5 ; D-2-amino-5-phosphonopentanoic acid ; CGP52432 ; 3-[[[(3 ; 4-dichlorophenyl)methyl]amino]propyl] (diethoxy-methyl) phosphinic acid ; DNQX ; 6 ; 7-dinitroquin
• 刊名：Brain Research Bulletin
• 出版年：2012
• 期刊代码：9_03619230
• 类别：neu
• 出版时间：1 August, 2012
• 卷：88
• 期：5
• 页码：529-533
• 文件大小：853 K

摘要

纬-Aminobutyric acid (GABA) is the principle inhibitory neurotransmitter in adult mammalian brain. GABA receptors B subtype (GABA_BRs) are abundantly expressed at presynaptic and postsynaptic neuronal structures in the rat ventrolateral periaqueductal gray (PAG), an area related to pain regulation. Activation of GABA_BRs by baclofen, a selective agonist, induces presynaptic inhibition by decreasing presynaptic glutamate release. At the same time, baclofen induces a postsynaptic inhibitory membrane current or potential. We here report that in the ventrolateral PAG, the postsynaptic inhibition is mediated by activation of G protein-coupled inwardly rectifying K⁺ (GIRK) channels. Blockade of K⁺ channels largely prevents postsynaptic action of baclofen. In contrast, presynaptic inhibition of baclofen is insensitive to K⁺ channel blockade. The data indicate that potassium channels play different roles in GABA_BR-mediated presynaptic and postsynaptic inhibition on PAG neurons.