Kodama T, Lai Y Y, Siegel J M
Dept. of Psychology, Tokyo Metropolitan Institute for Neuroscience, Fuchu, Japan.
Brain Res. 1998 Jan 5;780(1):178-81.
Anatomical studies and stimulation studies in the decerebrate animal have suggested that the muscle atonia of rapid eye movement (REM) sleep is mediated by a projection from cholinoceptive glutamatergic neurons in the pons to the nucleus magnocellularis (NMC) of medulla. This model suggests that glutamate release in NMC should be enhanced in REM sleep. In the present study, glutamate release across the sleep-wake cycle in NMC was measured by in vivo microdialysis. We found that glutamate release in NMC was significantly higher (p = 0.0252) during REM sleep than during wakefulness (W). Glutamate release during REM sleep was not elevated either in nucleus paramedianus (NPM) or in the pontine inhibitory area (PIA) regions where cholinergic stimulation suppresses muscle tone. Acetylcholine (ACh) microinjection into PIA enhanced glutamate release in NMC. These results support the hypothesis that a glutamatergic pathway from PIA to NMC is responsible for the suppression of muscle tone in REM sleep.
对去大脑动物的解剖学研究和刺激研究表明，快速眼动（REM）睡眠中的肌肉张力缺失是由脑桥中胆碱能感受性谷氨酸能神经元向延髓巨细胞网状核（NMC）的投射介导的。该模型表明，REM睡眠中NMC的谷氨酸释放应增强。在本研究中，通过体内微透析测量了NMC在睡眠-觉醒周期中的谷氨酸释放。我们发现，REM睡眠期间NMC中的谷氨酸释放显著高于清醒（W）期间（p = 0.0252）。在中旁核（NPM）或脑桥抑制区（PIA）中，胆碱能刺激抑制肌肉张力的区域，REM睡眠期间的谷氨酸释放也没有升高。向PIA微量注射乙酰胆碱（ACh）可增强NMC中的谷氨酸释放。这些结果支持了这样的假设，即从PIA到NMC的谷氨酸能通路负责REM睡眠中肌肉张力的抑制。
