Kimura K
Nihon Yakurigaku Zasshi. 1976 May;72(4):453-73. doi: 10.1254/fpj.72.453.
The role of 5HT and NA in the regulation of the sleep-awake cycle, especially in the triggering mechanisms of paradoxical sleep (PT), was studied in rabbits using reserpine, parachlorophenylalanine (PCPA), alpha-methyl-p-tyrosine (alpha-MT) and alpha-methyl -m-tyrosine (alpha-MMT). 1) Reserpine (0.5 mg/kg, i.v.) caused a diphasic action on the brain electrical activity in rabbits: an initial activation pattern in the EEG which continued to 2approximately3 hr, was followed gradually by a slow wave. Forty to sixty min after reserpine administration, spike waves resembling the PGO waves in cats appeared from the medial nucleus Trapezoides (Trap. m.) in rabbits. From the electrophysiological point of view, these spike waves (reserpine spike waves) were in many respects similar to those recorded during PS (TR spike waves). Later reserpine spike waves appeared almost continuously for about 8approximately12 hr during arousal and slow wave sleep stages. When the amplitude and grouping of spike waves became prominent, severe myoclonic jerky movements resembling "pseudo hallucinatory" behavior were observed. Polygrams of these periods were similar to those of PS except for abrupt arousal and orienting reactions. The onset of the typical PS episode was delayed by more than 8approximately9 hr. 2). Repeated doses of PCPA (500 mg/kg/day for 3 consecutive days, i.p.) caused only slight suppressive effect on slow wave sleep (SS), but spike waves similar to TR spike and/or reserpine spike waves developed throughout SS. When the amplitude and grouping of these spike waves were progressively increased, SS was often followed by PS. Abrupt enhancement of these spike waves as associated with "pseudo hallucinatory" behavior and aroused the animal. Usually these spike waves were not seen during arousal phase. When reserpine (0.5 mg/kg) was given i.v. to PCPA-treated rabbits, the latent period of appearance of reserpine spike waves was markedly shortened. 3) alpha-MMT, at a dose which had no effect on SS, markedly suppressed PS for a long period. These findings suggest that 5HT and NA in the lower brainstem play inhibitory roles on the triggering mechanism of PS.
利用利血平、对氯苯丙氨酸(PCPA)、α-甲基对酪氨酸(α-MT)和α-甲基间酪氨酸(α-MMT),在兔身上研究了5-羟色胺(5HT)和去甲肾上腺素(NA)在调节睡眠-觉醒周期中的作用,特别是在异相睡眠(PT)触发机制中的作用。1)利血平(0.5毫克/千克,静脉注射)对兔脑电活动产生双相作用:脑电图最初出现激活模式,持续约3小时,随后逐渐出现慢波。利血平给药后40至60分钟,兔内侧梯形核(Trap.m.)出现类似于猫的PGO波的棘波。从电生理学角度看,这些棘波(利血平棘波)在许多方面与异相睡眠期间记录到的棘波(TR棘波)相似。后来,在觉醒和慢波睡眠阶段,利血平棘波几乎持续出现约8至12小时。当棘波的振幅和成群现象变得明显时,观察到类似于“假性幻觉”行为的严重肌阵挛性抽搐运动。这些时期的多导睡眠图与异相睡眠的多导睡眠图相似,只是没有突然觉醒和定向反应。典型异相睡眠发作的起始延迟超过8至9小时。2)连续3天腹腔注射重复剂量的PCPA(500毫克/千克/天)对慢波睡眠(SS)仅产生轻微抑制作用,但在整个慢波睡眠期间会出现类似于TR棘波和/或利血平棘波的棘波。当这些棘波的振幅和成群现象逐渐增加时,慢波睡眠之后常常接着出现异相睡眠。这些棘波突然增强并伴有“假性幻觉”行为,使动物觉醒。通常在觉醒阶段看不到这些棘波。当给PCPA处理过的兔静脉注射利血平(0.5毫克/千克)时,利血平棘波出现的潜伏期明显缩短。3)α-MMT在对慢波睡眠无影响的剂量下,能长期显著抑制异相睡眠。这些发现表明,低位脑干中的5HT和NA对异相睡眠的触发机制起抑制作用。