Fenik Victor B, Davies Richard O, Kubin Leszek
Department of Animal Biology, 209E/VET, School of Veterinary Medicine, University of Pennsylvania, 3800 Spruce Street, Philadelphia, Pennsylvania 19104-6046, USA.
Am J Respir Crit Care Med. 2005 Nov 15;172(10):1322-30. doi: 10.1164/rccm.200412-1750OC. Epub 2005 Aug 11.
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.
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.
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.
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.
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.
对支配颏舌肌（一种上呼吸道扩张肌）的舌下（XII）运动神经元的研究表明，快速眼动睡眠期间上呼吸道运动张力的抑制是由去甲肾上腺素和5-羟色胺介导的兴奋作用减弱所引起的。
我们的目的是确定位于XII核区域的胺能受体的拮抗剂是否能消除XII运动神经元的快速眼动睡眠样无张力状态，以及是否需要5-羟色胺能和去甲肾上腺素能拮抗剂共同作用才能达到这一效果。
在向XII核微量注射哌唑嗪和麦角酰二乙胺的混合物或仅其中一种药物之前及之后的不同时间，通过脑桥注射卡巴胆碱在麻醉大鼠中诱发快速眼动睡眠样发作。
单独使用每种拮抗剂以及联合使用时，自发的XII神经活动均显著降低，降低幅度为35%至81%，这表明XII运动神经元受到去甲肾上腺素能和5-羟色胺能内源性兴奋驱动。在同时注射两种拮抗剂后的32至81分钟内，脑桥注射卡巴胆碱并未导致XII神经活动受到抑制，而其他特征性效应（海马和皮质脑电图激活以及呼吸频率减慢）仍然存在。随后，卡巴胆碱的抑制作用部分恢复，这与自发的XII神经活动从拮抗剂的抑制作用中恢复的情况平行。单独注射任何一种拮抗剂均未消除卡巴胆碱的抑制作用。
脑桥注射卡巴胆碱所诱导的XII运动神经元活动的快速眼动睡眠样抑制，可完全由去甲肾上腺素能和5-羟色胺能对XII运动神经元的联合作用减弱来解释。
