通过毒蕈碱受体在小鼠视交叉上核中引发的不依赖磷脂酶Cβ4的钙离子升高。

PLC beta 4-independent Ca2+ rise via muscarinic receptors in the mouse suprachiasmatic nucleus.

作者信息

Ikeda M, Sugiyama T, Suzuki K, Moriya T, Shibata S, Katsuki M, Allen C N, Yoshioka T

机构信息

Advanced Research Center for Human Sciences, School of Human Sciences, Waseda University, Saitama, Japan.

出版信息

Neuroreport. 2000 Apr 7;11(5):907-12. doi: 10.1097/00001756-200004070-00002.

DOI:10.1097/00001756-200004070-00002

PMID:10790853

Abstract

Cholinergic regulation of the suprachiasmatic nucleus (SCN) has been extensively studied although the intracellular signaling mechanisms are not well understood. We examined immunostaining for phospholipase C-beta (PLC-beta) families that couple to muscarinic acetylcholine receptors (mAChR) and demonstrated the expression of PLC-beta 1 and beta 4 in the mouse SCN. Ca2+ imaging analysis indicated that the MI-mAChR antagonist, pirenzepine blocked carbachol-induced Ca2+ elevation in the SCN and the response was equivalent between the wild type and the PLC-beta 4-knockout mice. In addition, the knockout mice displayed locomotor and temperature rhythms coupling to 24 h light/dark cycles. Therefore, it was proposed that PLC-beta 1 but not PLC-beta 4 was involved in the mAChR-mediated Ca2+ signaling in the SCN.

摘要

虽然对视交叉上核（SCN）的胆碱能调节已有广泛研究，但细胞内信号传导机制仍未完全明晰。我们检测了与毒蕈碱型乙酰胆碱受体（mAChR）偶联的磷脂酶C-β（PLC-β）家族的免疫染色情况，并证实了PLC-β1和β4在小鼠SCN中的表达。钙离子成像分析表明，M1-mAChR拮抗剂哌仑西平可阻断卡巴胆碱诱导的SCN中钙离子浓度升高，且野生型小鼠和PLC-β4基因敲除小鼠的反应相当。此外，基因敲除小鼠表现出与24小时明暗周期相耦合的运动和体温节律。因此，有人提出PLC-β1而非PLC-β4参与了SCN中mAChR介导的钙离子信号传导。