首页> 外文期刊>The Journal of Physiology >Melatonin modulates the light-induced sympathoexcitation and vagal suppression with participation of the suprachiasmatic nucleus in mice.
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Melatonin modulates the light-induced sympathoexcitation and vagal suppression with participation of the suprachiasmatic nucleus in mice.

机译:褪黑素在小鼠视交叉上核的参与下调节光诱导的交感神经兴奋和迷走神经抑制。

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In mammals, the autonomic nervous system mediates the central circadian clock oscillation from the suprachiasmatic nucleus (SCN) to the peripheral organs, and controls cardiovascular, respiratory and gastrointestinal functions. The present study was conducted in mice to address whether light signals conveyed to the SCN can control peripheral autonomic functions, and further examined the impact of centrally administered melatonin on peripheral autonomic functions via activation of melatonin receptor signalling. In vivo electrophysiological techniques were performed in anaesthetised, open-chest and artificially ventilated mice whilst monitoring the arterial blood pressure and heart rate. Light induced an increase of the renal sympathetic nerve activity, arterial blood pressure and heart rate immediately after lights on. Conversely, light rapidly suppressed the gastric vagal parasympathetic nerve activity, which was affected neither by hepatic vagotomy nor by total subdiaphragmatic vagotomy. These autonomic responses were mediated by the SCN since bilateral SCN lesion totally abolished the light-evoked neuronal and cardiovascular responses. Melatonin administered intracerebroventricularly (I.C.V.) attenuated the sympathetic and vagal nerve activities in a dose-dependent manner with a threshold of 0.1 ng and these effects were blocked by I.C.V. pre-treatment of the competitive melatonin receptor antagonist luzindole. These results suggest that light induces sympathoexcitation and vagal suppression through the SCN and that melatonin modulates the light-induced autonomic responses via activation of the central melatonin receptor signalling.
机译:在哺乳动物中,自主神经系统介导从上睑神经核(SCN)到周围器官的中央昼夜节律振荡,并控制心血管,呼吸和胃肠功能。本研究是在小鼠中进行的,目的是研究传递到SCN的光信号是否可以控制周围的自主神经功能,并进一步研究了通过褪黑激素受体信号传导对褪黑素进行集中给药对周围自主神经功能的影响。在麻醉,开胸和人工通气的小鼠中进行体内电生理技术,同时监测动脉血压和心率。点燃后立即点燃肾交感神经活动,动脉血压和心率增加。相反,光迅速抑制了胃迷走神经副交感神经活动,既不受肝迷走神经切断术,也不受全dia下迷走神经切断术的影响。这些自主反应是由SCN介导的,因为双侧SCN病变完全消除了光诱发的神经元和心血管反应。脑室内(I.C.V.)服用褪黑激素以剂量依赖性方式减弱交感神经和迷走神经活动,阈值为0.1 ng,这些作用被I.C.V.竞争性褪黑激素受体拮抗剂luzindole的预处理。这些结果表明,光通过SCN引起交感神经兴奋和迷走神经抑制,褪黑激素通过激活中央褪黑激素受体信号传导来调节光诱导的自主反应。

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