Kodama T, Lai Y Y, Siegel J M
VAMC, Sepulveda, CA 91343.
Brain Res. 1992 May 15;580(1-2):348-50. doi: 10.1016/0006-8993(92)90967-e.
Previous studies in our laboratory have found that muscle atonia could be triggered by two distinct areas of the medial medulla, a caudal region, corresponding to the nucleus paramedianus (NPM) and a rostral region, corresponding to the nucleus magnocellularis (NMC). The former region is responsive to acetylcholine (ACh) and the latter region is responsive to glutamate. In this study we have measured the endogenous ACh release across the sleep-wake cycle in these two areas with the microdialysis technique in unanesthetized, freely moving cats. We found that ACh release in NPM was state-dependent and was about 30% higher (P less than 0.001) during rapid eye movement (REM) sleep than during slow-wave sleep and wakefulness. However, ACh release in NMC was not selectively elevated in REM sleep. The enhancement of ACh release in NPM during REM sleep supports our hypothesis that ACh release onto cholinoceptive neurons in this area mediates the muscle atonia of REM sleep.
我们实验室之前的研究发现，延髓内侧的两个不同区域可引发肌肉张力缺失，一个是尾侧区域，对应旁正中核（NPM），另一个是头侧区域，对应巨细胞网状核（NMC）。前一个区域对乙酰胆碱（ACh）有反应，后一个区域对谷氨酸有反应。在本研究中，我们用微透析技术在未麻醉、自由活动的猫身上测量了这两个区域在睡眠-觉醒周期中的内源性ACh释放。我们发现，NPM中的ACh释放与睡眠状态有关，在快速眼动（REM）睡眠期间比在慢波睡眠和清醒时高约30%（P<0.001）。然而，NMC中的ACh释放在REM睡眠中并没有选择性升高。REM睡眠期间NPM中ACh释放的增强支持了我们的假设，即该区域向胆碱能感受神经元释放的ACh介导了REM睡眠中的肌肉张力缺失。
