Endogenous opiates in the nucleus tractus solitarius mediate electroacupuncture-induced sleep activities in rats.
Endogenous opiates in the nucleus tractus solitarius mediate electroacupuncture-induced sleep activities in rats.
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DOI：
10.1093/ecam/nep132
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发表时间：
2011
期刊：
影响因子：
--
通讯作者：
Chang FC
中科院分区：
文献类型：
--
作者：
Cheng CH;Yi PL;Lin JG;Chang FC
电针具有镇痛、抗炎、改善睡眠障碍等多种治疗作用。然而，电针改善睡眠的机制仍有待确定。在中国古代文献中已经指出，Anmian（EX 17）穴位是引发失眠的触发点之一。我们以前证明，电针刺激暗期大鼠的暗面穴可增强非快速眼动（NREM）睡眠，这涉及孤束核（NTS）胆碱能活动的诱导。除了孤束核的胆碱能激活外，内源性阿片系统的激活也可能是针刺影响睡眠的一种机制。因此，本研究的目的是调查参与的NTS阿片系统在EA诱导的睡眠改变。结果表明，电针暗期暗眠穴可增加大鼠NREM睡眠，但对快动眼睡眠无明显影响。在NTS内微量注射阿片受体拮抗剂纳洛酮和μ-阿片受体拮抗剂纳洛嗪可剂量依赖性地阻断NREM睡眠的增强;然而，δ-受体拮抗剂纳曲吲哚和κ-受体拮抗剂去甲binaltrophimine的给药并不影响EA诱导的睡眠改变。此外，电针刺激后，脑干和海马中的β-内啡肽显著增加，这一作用可被给予毒蕈碱拮抗剂东莨菪碱阻断。我们的研究结果表明，EA诱导的NREM睡眠增强的机制可能是介导的，部分通过胆碱能激活，刺激阿片能神经元，增加β-内啡肽的浓度和μ-阿片受体的参与。
Electroacupuncture (EA) possesses various therapeutic effects, including alleviation of pain, reduction of inflammation and improvement of sleep disturbance. The mechanisms of EA on sleep improvement, however, remain to be determined. It has been stated in ancient Chinese literature that the Anmian (EX17) acupoint is one of the trigger points that alleviates insomnia. We previously demonstrated that EA stimulation of Anmian acupoints in rats during the dark period enhances non-rapid eye movement (NREM) sleep, which involves the induction of cholinergic activity in the nucleus tractus solitarius (NTS). In addition to cholinergic activation of the NTS, activation of the endogenous opioidergic system may also be a mechanism by which acupuncture affects sleep. Therefore, this study was designed to investigate the involvement of the NTS opioidergic system in EA-induced alterations in sleep. Our present results indicate that EA of Anmian acupoints increased NREM sleep, but not rapid eye movement sleep, during the dark period in rats. This enhancement in NREM sleep was dose-dependently blocked by microinjection of opioid receptor antagonist, naloxone, and the μ-opioid receptor antagonist, naloxonazine, into the NTS; administrations of δ-receptor antagonist, natrindole, and the κ-receptor antagonist, nor-binaltrophimine, however, did not affect EA-induced alterations in sleep. Furthermore, β-endorphin was significantly increased in both the brainstem and hippocampus after the EA stimuli, an effect blocked by administration of the muscarinic antagonist scopolamine into the NTS. Our findings suggest that mechanisms of EA-induced NREM sleep enhancement may be mediated, in part, by cholinergic activation, stimulation of the opiodergic neurons to increase the concentrations of β-endorphin and the involvement of the μ-opioid receptors.
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影响因子：
4.5
作者：
FRANKEN, P;TOBLER, I;BORBELY, AA
通讯作者：
BORBELY, AA
影响因子：
7.6
作者：
FEINBERG, I;CAMPBELL, IG
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CAMPBELL, IG
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56.9
作者：
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通讯作者：
WALL, PD
影响因子：
3.3
作者：
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通讯作者：
NORGREN, R
影响因子：
3.3
作者：
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通讯作者：
Loewy, AD