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环磷酸腺苷(cAMP)和蛋白激酶A调节胆碱能快速眼动睡眠的产生。

cAMP and protein kinase A modulate cholinergic rapid eye movement sleep generation.

作者信息

Capece M L, Lydic R

机构信息

Department of Anesthesia, The Pennsylvania State University, College of Medicine, Hershey 17033, USA.

出版信息

Am J Physiol. 1997 Oct;273(4):R1430-40. doi: 10.1152/ajpregu.1997.273.4.R1430.

Abstract

Cholinergic neurotransmission in the medial pontine reticular formation (mPRF) modulates rapid eye movement (REM) sleep generation. Microinjection of cholinergic agonists and acetylcholinesterase inhibitors into the mPRF induces a REM sleep-like state, and microdialysis data reveal increased mPRF levels of acetylcholine during REM sleep. Muscarinic cholinergic receptors (mAChRs) participate in REM sleep generation, and data suggest that mAChRs of a non-M1 subtype modulate REM sleep generation. The signal transduction pathway activated by m2 and m4 mAChRs involves a pertussis toxin-sensitive G protein, adenylate cyclase (AC), adenosine 3',5'-cyclic monophosphate (cAMP), and protein kinase A (PKA). Therefore, the present study tested the hypothesis that cAMP and PKA within the mPRF modulate the carbachol-induced REM sleep-like state. To test this hypothesis, the mPRF was microinjected with compounds known to facilitate the effects of cAMP (dibutyryl cAMP and 8-bromo-cAMP), stimulate PKA (Sp-cAMP[S]), and inhibit PKA (Rp-cAMP[S]). The results showed that compounds that fostered the intracellular effects of cAMP significantly decreased cholinergic REM sleep, while having no effect on spontaneously occurring REM sleep. These data are consistent with the recent finding that within the mPRF, AC and a pertussis toxin-sensitive G protein modulate cholinergic REM sleep generation. These new data suggest a modulatory role for pontine cAMP and PKA in cholinergic REM sleep regulation.

摘要

脑桥内侧网状结构(mPRF)中的胆碱能神经传递调节快速眼动(REM)睡眠的产生。向mPRF微量注射胆碱能激动剂和乙酰胆碱酯酶抑制剂可诱导出类似REM睡眠的状态,微透析数据显示REM睡眠期间mPRF中的乙酰胆碱水平升高。毒蕈碱型胆碱能受体(mAChRs)参与REM睡眠的产生,数据表明非M1亚型的mAChRs调节REM睡眠的产生。由m2和m4 mAChRs激活的信号转导途径涉及一种对百日咳毒素敏感的G蛋白、腺苷酸环化酶(AC)、3',5'-环磷酸腺苷(cAMP)和蛋白激酶A(PKA)。因此,本研究检验了以下假设:mPRF内的cAMP和PKA调节卡巴胆碱诱导的类似REM睡眠的状态。为了验证这一假设,向mPRF微量注射已知可促进cAMP作用的化合物(二丁酰cAMP和8-溴-cAMP)、刺激PKA的化合物(Sp-cAMP[S])以及抑制PKA的化合物(Rp-cAMP[S])。结果表明,促进cAMP细胞内效应的化合物显著减少胆碱能REM睡眠,而对自发出现的REM睡眠无影响。这些数据与最近的一项发现一致,即在mPRF内,AC和一种对百日咳毒素敏感的G蛋白调节胆碱能REM睡眠的产生。这些新数据表明脑桥cAMP和PKA在胆碱能REM睡眠调节中具有调节作用。

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