Terao A, Matsumura H, Yoneda H, Saito M
Department of Molecular Behavioural Biology, Osaka Bioscience Institute, Suita City, Japan.
Neuroreport. 1998 Dec 1;9(17):3791-6. doi: 10.1097/00001756-199812010-00005.
Tumor necrosis factor-alpha (TNFalpha) was infused into the subarachnoid space of the rat rostral basal forebrain, which was previously defined as a prostaglandin (PG) D2-sensitive, sleep-promoting zone. TNFalpha increased the amount of slow-wave sleep (SWS), decreased that of paradoxical sleep (PS), and caused fever and anorexia. The TNFalpha-induced SWS enhancement, fever and anorexia were all blocked by co-infusion of diclofenac, a non-selective cyclooxygenase (COX) inhibitor, and by pretreatment with NS-398, a COX-2-specific inhibitor. In striking contrast, the TNFalpha-induced suppression of PS was not affected by the inhibitors. These results indicate that COX-2-mediated hyperproduction of PGs is critically involved in the enhancement of SWS, fever, and anorexia but not in the suppression of PS, caused by TNFalpha infused into the PGD2-sensitive zone.
将肿瘤坏死因子-α（TNFα）注入大鼠前脑基底部蛛网膜下腔，该区域先前被定义为对前列腺素（PG）D2敏感的促睡眠区。TNFα增加了慢波睡眠（SWS）的量，减少了异相睡眠（PS）的量，并引起发热和厌食。TNFα诱导的SWS增强、发热和厌食均被非选择性环氧化酶（COX）抑制剂双氯芬酸的共同注入以及COX-2特异性抑制剂NS-398的预处理所阻断。与之形成鲜明对比的是，TNFα诱导的PS抑制不受这些抑制剂的影响。这些结果表明，COX-2介导的PG过度产生在TNFα注入PGD2敏感区所引起的SWS增强、发热和厌食中起关键作用，但在PS抑制中不起作用。
