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在大鼠交感神经元中,通过Gαq/11抑制毒蕈碱M电流以及通过Gαo抑制α-肾上腺素能受体对Ca2+电流的作用。

Muscarinic M-current inhibition via G alpha q/11 and alpha-adrenoceptor inhibition of Ca2+ current via G alpha o in rat sympathetic neurones.

作者信息

Caulfield M P, Jones S, Vallis Y, Buckley N J, Kim G D, Milligan G, Brown D A

机构信息

Wellcome Laboratory for Molecular Pharmacology, Department of Pharmacology, University College London.

出版信息

J Physiol. 1994 Jun 15;477 ( Pt 3)(Pt 3):415-22. doi: 10.1113/jphysiol.1994.sp020203.

DOI:10.1113/jphysiol.1994.sp020203
PMID:7932231
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1155606/
Abstract
  1. Microinjection of selective antibodies into superior cervical ganglion (SCG) neurones has identified the G-protein alpha-subunits mediating muscarinic receptor inhibition of M-type K+ current (IK(M)) and alpha-adrenoceptor inhibition of Ca2+ current (ICa). 2. Antibodies specific for G alpha q/11, but not those for G alpha o, reduced M-current inhibition by the muscarinic agonist oxotremorine-M, whereas anti-G alpha o antibodies, but not anti-G alpha q/11 or anti-G alpha i1-3 antibodies, reduced calcium current inhibition by noradrenaline. 3. Immunoblots with specific anti-G-protein antibodies demonstrated the presence of both G alpha q and G alpha 11, while G alpha o1 (but virtually no G alpha o2) was present. 4. We conclude that M1 muscarinic receptor inhibition of IK(M) is transduced by G alpha q and/or G alpha 11, and that G alpha o transduces alpha-adrenoceptor inhibition of ICa.
摘要
  1. 向上颈神经节(SCG)神经元微量注射选择性抗体,已鉴定出介导毒蕈碱受体对M型钾电流(IK(M))抑制作用的G蛋白α亚基,以及介导α肾上腺素能受体对钙电流(ICa)抑制作用的G蛋白α亚基。2. 对Gαq/11特异的抗体可减弱毒蕈碱激动剂氧化震颤素-M对M电流的抑制作用,而对Gαo特异的抗体则不能;相反,对Gαo特异的抗体可减弱去甲肾上腺素对钙电流的抑制作用,而对Gαq/11或Gαi1-3特异的抗体则不能。3. 用特异的抗G蛋白抗体进行免疫印迹分析表明,同时存在Gαq和Gα11,且存在Gαo1(但几乎不存在Gαo2)。4. 我们得出结论,M1毒蕈碱受体对IK(M)的抑制作用是由Gαq和/或Gα11介导的,而Gαo介导α肾上腺素能受体对ICa的抑制作用。
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09c5/1155606/3f844b195f47/jphysiol00350-0050-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09c5/1155606/f52fe6d1cbd4/jphysiol00350-0049-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09c5/1155606/3f844b195f47/jphysiol00350-0050-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09c5/1155606/f52fe6d1cbd4/jphysiol00350-0049-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09c5/1155606/3f844b195f47/jphysiol00350-0050-a.jpg

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