OXIDIZED GLUTATHIONE REGULATES PHYSIOLOGICAL SLEEP IN UNRESTRAINED RATS
OXIDIZED GLUTATHIONE REGULATES PHYSIOLOGICAL SLEEP IN UNRESTRAINED RATS
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DOI：
10.1016/0006-8993(94)91024-3
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发表时间：
1994-02-14
期刊：
影响因子：
2.9
通讯作者：
INOUE, S
中科院分区：
文献类型：
--
作者：
HONDA, K;KOMODA, Y;INOUE, S
氧化型谷胱甘肽（Oxidized glutathione，GSSG）是从24 h睡眠剥夺大鼠脑干中提取的睡眠促进物质（sleep-promoting substance，SPS）的活性成分。我们分析了五种剂量的GSSG在不受限制的大鼠中的催眠和体温调节活性。夜间10小时脑室注射GSSG显着增强慢波睡眠（SWS）的剂量范围从20到50 nmol和异相睡眠（PS）在25 nmol的代价在清醒期间的12小时黑暗期。SWS和PS的剂量-反应关系均呈钟形。25 nmol/10 h GSSG给药诱导夜间睡眠总时间最大增加（SWS为基线以上35%，PS为86%）。睡眠的增强主要是由于SWS发作持续时间和PS发作次数的增加。GSSG在25 nmol/10 h引起脑温度（T-脑）的显着波动，双相低温和高热反应在输液期间，随后由高热状态在随后的恢复日的光照期间，然后在黑暗期间的低温状态。根据GSSG对大鼠脑兴奋性突触膜的抑制作用，我们推测GSSG的促睡眠作用是通过对脑内兴奋性神经传递的生理调节而引起的。
Oxidized glutathione (GSSG) is an active component of sleep-promoting substance (SPS) which was originally extracted from the brainstems of 24-h sleep-deprived rats. We analyzed somnogenic and thermoregulatory activities of five doses of GSSG in unrestrained rats. A nocturnal 10-h intracerebroventricular infusion of GSSG significantly enhanced slow wave sleep (SWS) at the dosage range from 20 to 50 nmol and paradoxical sleep (PS) at 25 nmol at the expense of wakefulness during the 12-h dark period. The dose-response relations exhibited a bell shape for both SWS and PS. The administration of 25 nmol/10 h GSSG induced the maximal increase in the total time of nocturnal sleep (35% above the baseline for SWS and 86% for PS). The enhancement of sleep was mainly due to an increase in the duration of SWS episodes and in the number of PS episodes. GSSG at 25 nmol/10 h elicited significant fluctuations in brain temperature (T-brain), biphasic hypothermal and hyperthermal reactions during the infusion period, followed by a hyperthermal state during the subsequent light period of the recovery day and then a hypothermal state during the dark period. On the basis of recent literature on the inhibitory action of GSSG on the excitatory synaptic membrane of rat brain, we speculate that the sleep-enhancing activity of GSSG was caused by its physiological modulation on the glutamatergic neurotransmission in the brain.