Hayaishi Osamu
Osaka Bioscience Institute, Suita, Osaka 565-0874, Japan.
J Appl Physiol (1985). 2002 Feb;92(2):863-8. doi: 10.1152/japplphysiol.00766.2001.
To elucidate the exact role of the PGD(2) system in sleep-wake regulation in vivo, the sleep behavior of knockout mice, generated in the author's and other laboratories, was examined for lipocalin-type PGD synthase (L-PGDS), PGD receptor, adenosine A(2A) receptor, and histamine H(1) receptor; transgenic mice overexpressing the human L-PGDS gene, generated in the author's laboratory, were also examined. The circadian profiles of sleep patterns of wild-type and the genetically manipulated mice were essentially identical, indicating the possibility that the deficiency of one system may be effectively compensated by some other systems during development. Available evidence indicated that the PGD(2) system is involved in the homeostatic regulation of non-rapid eye movement sleep and that the arousal effect of orexin A is mediated by the histamine H(1) receptor system.
为了阐明前列腺素D2（PGD(2)）系统在体内睡眠-觉醒调节中的确切作用，对作者所在实验室及其他实验室培育的基因敲除小鼠的睡眠行为进行了检测，检测对象包括脂质运载蛋白型PGD合酶（L-PGDS）、PGD受体、腺苷A(2A)受体和组胺H(1)受体；还检测了作者所在实验室培育的过表达人L-PGDS基因的转基因小鼠。野生型小鼠和基因操作小鼠睡眠模式的昼夜节律基本相同，这表明在发育过程中一个系统的缺陷可能会被其他一些系统有效补偿。现有证据表明，PGD(2)系统参与非快速眼动睡眠的稳态调节，且食欲素A的觉醒作用由组胺H(1)受体系统介导。
