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抗白细胞介素-1β可减少大鼠睡眠剥夺后的睡眠及睡眠反弹。

Anti-interleukin-1 beta reduces sleep and sleep rebound after sleep deprivation in rats.

作者信息

Opp M R, Krueger J M

机构信息

Department of Physiology and Biophysics, University of Tennessee, Memphis 38163.

出版信息

Am J Physiol. 1994 Mar;266(3 Pt 2):R688-95. doi: 10.1152/ajpregu.1994.266.3.R688.

DOI:10.1152/ajpregu.1994.266.3.R688
PMID:8160860
Abstract

Interleukin-1 (IL-1) is somnogenic and is hypothesized to be involved in physiological sleep regulation. Antibodies directed against rat IL-1 beta were used to further elucidate possible contributions of IL-1 to sleep regulation. Rabbit anti-rat IL-1 beta (anti-IL-1 beta) was injected intracerebroventricularly into normal rats 15 min before light onset. A 20-microgram dose of anti-IL-1 beta reduced non-rapid-eye-movement (NREM) sleep by 60 min during the subsequent 12-h slight period. There was no effect on rapid eye movement sleep after this dose of anti-IL-1 beta. The effects of anti-IL-1 beta on the enhancement of sleep after periods of sleep deprivation were also determined. When rats were deprived of sleep for 3-h beginning at light onset, the amount of time spent in NREM sleep increased for the remaining 9 h of the light period, regardless of whether control intracerebroventricular injections of pyrogen-free saline or rabbit immunoglobulin G were given during the deprivation period. However, when 20 micrograms anti-IL-1 beta were injected intracerebroventricularly during the sleep deprivation period, the expected NREM sleep rebound was completely blocked. Collectively, these data provide additional support for the hypothesis that IL-1 is involved in regulation of physiological sleep-wake activity.

摘要

白细胞介素-1(IL-1)具有诱导睡眠的作用,据推测其参与生理睡眠调节。使用针对大鼠IL-1β的抗体来进一步阐明IL-1对睡眠调节可能产生的作用。在光照开始前15分钟,将兔抗大鼠IL-1β(抗IL-1β)脑室内注射到正常大鼠体内。20微克剂量的抗IL-1β在随后12小时的光照期内使非快速眼动(NREM)睡眠减少了60分钟。该剂量的抗IL-1β对快速眼动睡眠没有影响。还确定了抗IL-1β对睡眠剥夺后睡眠增强的影响。当大鼠从光照开始时被剥夺3小时睡眠,无论在剥夺期内脑室内注射无热原生理盐水或兔免疫球蛋白G作为对照,在光照期剩余的9小时内,NREM睡眠的时长都会增加。然而,当在睡眠剥夺期脑室内注射20微克抗IL-1β时,预期的NREM睡眠反弹被完全阻断。总体而言,这些数据为IL-1参与生理睡眠-觉醒活动调节这一假说提供了更多支持。

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