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毒蕈碱受体介导了卡巴胆碱诱导的叙利亚仓鼠昼夜活动节律的相位偏移。

Muscarinic receptors mediate carbachol-induced phase shifts of circadian activity rhythms in Syrian hamsters.

作者信息

Bina K G, Rusak B

机构信息

Department of Psychology, Dalhousie University, Halifax, Nova Scotia, Canada.

出版信息

Brain Res. 1996 Dec 16;743(1-2):202-11. doi: 10.1016/s0006-8993(96)01043-8.

DOI:10.1016/s0006-8993(96)01043-8
PMID:9017247
Abstract

Carbachol, a non-specific cholinergic agonist, when administered intraventricularly or directly into the suprachiasmatic nucleus (SCN), causes phase-dependent shifts in circadian rhythms of wheel-running activity in rodents. The cholinergic receptor subtype involved in mediating these carbachol-induced phase shifts, however, remains uncertain. In order to investigate this issue we injected carbachol into the SCN through indwelling cannulas at circadian times (CT) 6, 14 and 22 in Syrian hamsters (Mesocricetus auratus) maintained in constant darkness. Carbachol elicited large phase advances at CT 6 (69.8 +/- 15.7 min; mean +/- S.E.M.) and CT 22 (83.9 +/- 24.8 min) and phase delays at CT 14 (59.7 +/- 18 min). We attempted to block the carbachol-induced phase shifts at these three phases using specific antagonists of nicotinic and muscarinic receptors. Mecamylamine, a nicotinic receptor antagonist, did not block carbachol-induced phase shifts at any of the phases tested. Atropine, a muscarinic receptor antagonist, blocked carbachol-induced phase shifts at CT 6 (-11.6 +/- 4.8 min; Mean phase shift +/- S.E.M.) and CT 22 (-20 +/- 6.6 min), suggesting that carbachol mediates its phase-shifting effects at these phases through muscarinic receptors.

摘要

卡巴胆碱是一种非特异性胆碱能激动剂,当脑室内注射或直接注入视交叉上核(SCN)时,会导致啮齿动物转轮活动的昼夜节律发生相位依赖性变化。然而,介导这些卡巴胆碱诱导的相位变化所涉及的胆碱能受体亚型仍不确定。为了研究这个问题,我们在持续黑暗环境下饲养的叙利亚仓鼠(金仓鼠)的昼夜时间(CT)6、14和22时,通过留置套管将卡巴胆碱注入SCN。卡巴胆碱在CT 6(69.8±15.7分钟;平均值±标准误)和CT 22(83.9±24.8分钟)时引起大幅相位提前,在CT 14时引起相位延迟(59.7±18分钟)。我们试图使用烟碱样和毒蕈碱样受体的特异性拮抗剂来阻断这三个阶段的卡巴胆碱诱导的相位变化。烟碱样受体拮抗剂美加明在任何测试阶段都不能阻断卡巴胆碱诱导的相位变化。毒蕈碱样受体拮抗剂阿托品在CT 6(-11.6±4.8分钟;平均相位变化±标准误)和CT 22(-20±6.6分钟)时阻断了卡巴胆碱诱导的相位变化,这表明卡巴胆碱在这些阶段通过毒蕈碱样受体介导其相位变化作用。

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