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作 者:朱国庆[1] 钟明奎[1] 张景行[1] 赵乐章[1] 章功良[1] 高隽[1]
出 处:《中国神经科学杂志》1999年第4期306-311,共6页
基 金:安徽省自然科学基金!资助项目(95-医药-06)
摘 要:应用多道睡眠描记术(PSG)研究大鼠基底外侧杏仁核(BLN)在睡眠-觉醒调节中的作用与机制。双侧BLN 内微量注射损毁神经元胞体剂量的海人酸(KA)立即引起不眠状态,自第3 天开始慢波睡眠(SWS)增多,但快波睡眠(PS)不受影响。单侧BLN内注射吗啡引起慢波睡眠抑制效应,而阿片受体阻断剂纳洛酮促进SWS并可阻断吗啡的效应。环磷酸腺苷(cAMP)增加SWS,但环磷酸鸟苷(cGMP)减少SWS。鸟苷酸环化酶抑制剂亚甲蓝的效应与cGMP相反。本研究表明BLN内阿片机制在睡眠-觉醒调节中具有重要作用,内源性阿片样物质抑制SWS,这一作用可能是通过cGMP增多或cAMP减少实现的。The role and mechanism of basolateral amygdaloid nucleus (BLN) in sleep and wakefulness were investigated with polysomnography (PSG) in rats. Bilateral microinjection of kainic acid (KA) into BLN to destroy neurons caused sleepless status immediately. From the third day , slow wave sleep (SWS) increased, but paradoxical sleep (PS) did not change. Unilateral microinjection of morphine resulted in a SWS inhibiting effect. Naloxone, an opioid receptor blocker, promoted SWS and blocked the effect of morphine. Cyclic AMP increased SWS, but cyclic GMP decreased SWS. Methylene blue, an inhibitor of guanylate cyclase, caused contrary effect to cGMP. The present results indicated that opioid mechanism in BLN played an important role in sleep regulation, and that endogenous opioid like substances inhibited SWS, which was probably mediated by the increase of cGMP or the decrease of cAMP concentration.
分 类 号:R338.63[医药卫生—人体生理学] R338.26[医药卫生—基础医学]
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