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目的内源性前列腺素(prostaglandin,PG)D2能增加基底前脑下蛛网膜下腔内的腺苷水平,可能作用于腺苷A2A受体,诱发睡眠。本实验观察腺苷A2A受体特异性激动剂CGS21680和PGD2促眠作用的异同。方法手术插入不锈钢导管至大鼠基底前脑下蛛网膜下腔,同时埋植脑电波和肌电波记录电极,术后2周,经导管微量恒速灌注PGD2(200pmol·0.2μL-1·min-1)或CGS21680(10pmol·0.2μL-1·min-1),同步记录脑电波和肌电波,分析睡眠量、睡眠强度及睡眠时相转换等参数。结果与人工脑脊液自身对照相比,PGD2和CGS21680都显著增加慢波睡眠(非快动眼睡眠)量和睡眠强度,两者在时相转化和各波段时程上表现出高度的相似性。CGS21680增加快动眼睡眠量,而PGD2不引起快动眼睡眠量的增加。结论腺苷A2A受体激动剂CGS21680能模拟PGD2诱发的慢波睡眠,提示腺苷A2A受体是诱导生理性睡眠的重要靶点之一。
Objective Endogenous prostaglandin (D2) D2 can increase the level of adenosine in subbasal subarachnoid space of basal forebrain, which may act on adenosine A2A receptor and induce sleep. The experiment observed adenosine A2A receptor specific agonist CGS21680 and PGD2 similarities and differences in the role of sleep. Methods The stainless steel catheter was inserted into the subarachnoid space of the basilar membrane in the basilar artery of the rats. EEG and EMG recording electrodes were implanted at the same time. PGD2 (200 pmol · 0.2 μL-1 · min- 1), or CGS21680 (10 pmol·0.2 μL -1·min -1). The parameters of sleep volume, sleep intensity and phase transition during sleep were analyzed. Results Both PGD2 and CGS21680 significantly increased the amount of slow-wave sleep (non-REM sleep) and sleep intensity compared with artificial cerebrospinal fluid self-control, both of which displayed a high degree of similarity in the phase transition and the time-history of each wave band. CGS21680 increased the amount of fast eye movement sleep, while PGD2 did not cause an increase in fast eye movement sleep volume. Conclusion Adenosine A2A receptor agonist CGS21680 can simulate PGD2-induced slow wave sleep, suggesting that adenosine A2A receptor is one of the important targets for inducing physiological sleep.