González M M, Valatx J L
Département de Médecine Expérimentale, INSERM U480, Faculté de Médecine, Université Claude Bernard, Lyon, France.
Behav Pharmacol. 1998 Dec;9(8):655-62. doi: 10.1097/00008877-199812000-00001.
A previous study demonstrated the efficacy of the corticotropin-releasing hormone (CRH) receptor antagonist, alpha-helical CRH (9-41), in blocking the paradoxical sleep increase induced by stress. In the present study, this peptide was used to evaluate the involvement of the stress component of the sleep deprivation, in the paradoxical sleep rebound. Rats were subjected for 10 h to the classical water-tank sleep-deprivation technique and were given, every 2 h throughout the sleep deprivation period, intracerebroventricular injections of either 100 microg/5 microl of alpha-helical CRH (9-41) or vehicle alone. Continuous recordings showed that antagonist treatment decreased the PS rebound, but not the SWS rebound, following sleep deprivation. These findings suggest that, in the water-tank sleep deprivation method, stress, acting via CRH activation, is the main factor inducing the paradoxical sleep rebound.
先前的一项研究证明,促肾上腺皮质激素释放激素(CRH)受体拮抗剂α-螺旋CRH(9-41)在阻断应激诱导的异相睡眠增加方面具有功效。在本研究中,使用该肽来评估睡眠剥夺应激成分在异相睡眠反弹中的作用。大鼠采用经典的水槽睡眠剥夺技术剥夺睡眠10小时,并在整个睡眠剥夺期间每2小时进行一次脑室内注射,注射的要么是100微克/5微升的α-螺旋CRH(9-41),要么是单独的赋形剂。连续记录表明,拮抗剂处理可减少睡眠剥夺后的异相睡眠反弹,但不影响慢波睡眠反弹。这些发现表明,在水槽睡眠剥夺方法中,通过CRH激活起作用的应激是诱导异相睡眠反弹的主要因素。