Taguchi O, Kubin L, Pack A I
Center for Sleep and Respiratory Neurobiology, University of Pennsylvania, Philadelphia 19104.
Brain Res. 1992 Nov 6;595(1):107-15. doi: 10.1016/0006-8993(92)91458-q.
To study mechanisms underlying the postural muscle atonia and respiratory depression associated with rapid eye movement (REM) sleep, the cholinergic agonist, carbachol, was microinjected into the pontine reticular formation in decerebrate, spontaneously breathing rats. Carbachol injection led to a simultaneous depression of neck and tonic intercostal EMG activity (lasting 14.5 min +/- 7.6 (S.D.)) and a reduction of the respiratory rate. Phasic inspiratory intercostal activity was not consistently depressed. After a spontaneous recovery from the atonia and respiratory depression, subsequent carbachol injections at the same site produced similar responses. Thus, the decerebrate rat may provide a useful model for studies of the inhibitory neural mechanisms activated by the increased acetylcholine levels in the pons that occur in REM sleep. Pontine carbachol effects in rats differ from those described in cats in a manner analogous to differences in the patterns of natural REM sleep in these two species.
为研究与快速眼动(REM)睡眠相关的姿势性肌肉张力缺失和呼吸抑制的潜在机制,将胆碱能激动剂卡巴胆碱微量注射到去大脑、自主呼吸的大鼠脑桥网状结构中。注射卡巴胆碱导致颈部和强直性肋间肌肌电图活动同时受到抑制(持续14.5分钟±7.6(标准差)),且呼吸频率降低。阶段性吸气肋间肌活动并未持续受到抑制。从肌张力缺失和呼吸抑制状态自然恢复后,在同一部位再次注射卡巴胆碱会产生类似反应。因此,去大脑大鼠可能为研究REM睡眠时脑桥中乙酰胆碱水平升高所激活的抑制性神经机制提供一个有用的模型。大鼠脑桥注射卡巴胆碱的效应与猫的不同,这与这两个物种自然REM睡眠模式的差异类似。