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Kappa-Opioid Receptors in the Caudal Nucleus Tractus Solitarius Mediate 100 Hz Electroacupuncture-Induced Sleep Activities in Rats

机译:尾核中的κ阿片受体介导100 MediaHz电针诱导的大鼠睡眠活动

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摘要

Previous results demonstrated that 10 Hz electroacupuncture (EA) of Anmian acupoints in rats during the dark period enhances slow wave sleep (SWS), which involves the induction of cholinergic activity in the caudal nucleus tractus solitarius (NTS) and subsequent activation of opioidergic neurons and μ-receptors. Studies have shown that different kinds of endogenous opiate peptides and receptors may mediate the consequences of EA with different frequencies. Herein, we further elucidated that high-frequency (100 Hz)-EA of Anmian enhanced SWS during the dark period but exhibited no direct effect on rapid eye movement (REM) sleep. High-frequency EA-induced SWS enhancement was dose-dependently blocked by microinjection of naloxone or κ-receptor antagonist (nor-binaltorphimine) into the caudal NTS, but was affected neither by μ- (naloxonazine) nor δ-receptor antagonists (natatrindole), suggesting the role of NTS κ-receptors in the high-frequency EA-induced SWS enhancement. Current and previous results depict the opioid mechanisms of EA-induced sleep.
机译:先前的研究结果表明,在黑暗时期,大鼠安眠穴的10 Hz电针(EA)会增强慢波睡眠(SWS),这包括在孤尾尾孤核(NTS)中诱导胆碱能活性并随后激活视皮膜神经元和μ受体。研究表明,不同种类的内源性阿片肽和受体可能以不同的频率介导EA的后果。在本文中,我们进一步阐明了安眠的高频(100 Hz)-EA在黑暗时期增强了SWS,但对快速眼动(REM)睡眠没有直接影响。通过将纳洛酮或κ受体拮抗剂(去甲双萘酚胺)显微注射到尾部NTS中,剂量依赖性地阻止了高频EA诱导的SWS增强,但是μ-(纳洛嗪嗪)或δ受体拮抗剂(那曲三烯)均未对其产生影响。 ,提示NTSκ受体在高频EA诱导的SWS增强中的作用。当前和以前的结果描述了EA诱导的睡眠的阿片类药物机制。

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