REM sleep-like atonia of hypoglossal (XII) motoneurons is caused by loss of noradrenergic and serotonergic inputs
REM sleep-like atonia of hypoglossal (XII) motoneurons is caused by loss of noradrenergic and serotonergic inputs
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DOI：
10.1164/rccm.200412-1750oc
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发表时间：
2005-11-15
影响因子：
24.7
通讯作者：
Kubin, L
中科院分区：
文献类型：
--
作者：
Fenik, VB;Davies, RO;Kubin, L
理由：对支配颏舌肌（一种上气道扩张器）的舌下 (XII) 运动神经元的研究表明，快速眼动睡眠期间上气道运动音调的抑制是由去甲肾上腺素和血清素介导的兴奋取消引起的。 目的：我们的目标是确定位于 XII 核区域的胺能受体的拮抗作用是否可以消除 XII 的快速眼动睡眠样肌张力障碍。方法：在将哌唑嗪和美西麦角组合或仅其中一种药物微注射到 XII 核之前和之后的不同时间，通过注射桥脑卡巴胆碱，在麻醉大鼠中引发快速眼动睡眠样发作。测量和主要结果：自发性 XII 神经活动显着降低，每种拮抗剂单独使用和组合使用时增加了 35% 至 81%，表明 XII 运动神经元同时受到去甲肾上腺素能和血清素能内源性兴奋驱动。在显微注射两种拮抗剂后的 32 至 81 分钟内，桥脑卡巴胆碱没有引起 XII 神经活动的抑制，而其他特征效应（海马和皮质脑电图的激活以及呼吸频率的减慢）保持不变。然后，卡巴胆碱的抑制作用部分恢复，同时自发的XII神经活动从拮抗剂的抑制作用中恢复。单独显微注射任一拮抗剂均不能消除卡巴胆碱的抑制作用。结论：桥脑卡巴胆碱引起的 XII 运动神经元活动的快速眼动睡眠样抑制可以完全通过去甲肾上腺素能和血清素能对 XII 运动神经元的作用的联合撤消来解释。
Rationale: Studies of hypoglossal (XII) motoneurons that innervate the genioglossus muscle, an upper airway dilator, suggested that the suppression of upper airway motor tone during REM sleep is caused by withdrawal of excitation mediated by norepinephrine and serotonin.Objectives: Our objectives were to determine whether antagonism of aminergic receptors located in the XII nucleus region can abolish the REM sleep-like atonia of XII motoneurons, and whether both serotonergic and noradrenergic antagonists are required to achieve this effect.Methods: REM sleep-like episodes were elicited in anesthetized rats by Pontine carbachol injections before and at various times after microinjection of prazosin and methysergide combined, or of only one of the drugs, into the XII nucleus.Measurements and Main Results: Spontaneous XII nerve activity was significantly reduced, by 35 to 81%, by each antagonist alone and in combination, indicating that XII motoneurons were under both noradrenergic and serotonergic endogenous excitatory drives. During the 32 to 81 min after microinjections of both antagonists, pontine carbachol caused no depression of XII nerve activity, whereas other characteristic effects (activation of the hippocampal and cortical EEG, and slowing of the respiratory rate) remained intact. A partial recovery of the depressant effect of carbachol then occurred parallel to the recovery of spontaneous XII nerve activity from the depressant effect of the antagonists. Microinjections of either antagonist alone did not eliminate the depressant effect of carbachol.Conclusions: The REM sleep-like depression of XII motoneuronal activity induced by Pontine carbachol can be fully accounted for by the combined withdrawal of noradrenergic and serotonergic effects on XII motoneurons.