Comparison of the three mouse G-protein-activated K+ (GIRK) channels and functional couplings of the opioid receptors with the GIRK1 channel

Comparison of the three mouse G-protein-activated K+ (GIRK) channels and functional couplings of the opioid receptors with the GIRK1 channel
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DOI:
10.1111/j.1749-6632.1996.tb17434.x
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发表时间:
1996-01-01
期刊:
CELLULAR AND MOLECULAR MECHANISMS OF DRUGS OF ABUSE
影响因子:
--
通讯作者:
Kumanishi, T
Kumanishi, T
中科院分区:
其他
文献类型:
--
作者:
Ikeda, K;Kobayashi, T;Kumanishi, T

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阿片、多巴胺和5-羟色胺受体是药物成瘾的关键分子。先前对这些受体的信号转导途径的研究表明,它们的激活改变了K+和Ca*+的膜电导以及第二信使如cAMP和1,4,5-三磷酸的水平,每一个都是通过G蛋白激活的,最终导致神经放电和神经递质释放的激活或抑制。在这些受体的信号转导中,G蛋白激活的K+通道(GIRK通道)被认为发挥着重要的作用,它是内向整流钾通道家族的成员之一。最近的分子生物学研究揭示了大脑中至少存在三种GIRK通道,GIRK1,GIRK2和GIRK3通道。然而,这些GIRK通道的细节,包括它们彼此之间的体内关系以及它们与各种受体的功能偶联,在很大程度上仍不清楚。A这项工作部分得到了日本文部科学省和RIKEN前沿研究计划的研究资助。通讯作者:池田和隆,突触功能实验室,前沿性研究项目,理化学研究所,广泽2-1,Wako,Saitama,351-01,日本。电话:+81-48-462-1111(分机:3102);
The opioid, dopamine and serotonin receptors are crucial molecules in drug addictions. Previous studies of signal transduction pathways from these receptors have shown that their activation alters membrane conductances for K+ and Ca*+ and levels of second messengers such as CAMP and inositol 1, 4, 5-triphosphate, each through G-protein activation, and ultimately results in the activation or inhibition of neural firing and of neurotransmitter release.'In the signal transduction from these receptors, the G-protein-activated K+ channel (GIRK channel), a member of a family of inward-rectifier K+ channels, is considered to play an important r~ le.~,~ Recent molecular biological studies have revealed the presence of at least three GIRK channels in the brain, GIRK1, GIRK2 and GIRK3 channels. 5-* However, details of these GIRK channels including those regarding their in vivo relationships among each other and their functional coupling with various receptors remain largely unknown. a This work was supported in part by research grants from the Ministry of Education, Science and Culture of Japan and the Frontier Research Program, RIKEN. Corresponding author: Kazutaka Ikeda, Laboratory for Synaptic Function, Frontier Research Program, the Institute of Physical and Chemical Research (RIKEN), Hirosawa 2-1, Wako, Saitama 351-01, Japan. Tel.:+ 81-48-462-1111 (ext: 3102); Fax:+ 81-48-462-4798;