Lin J S, Sakai K, Jouvet M
Département de Médicine Expérimentale, INSERM U52, CNRS UA 1195, Université Claude Bernard, Lyon, France.
Neuropharmacology. 1988 Feb;27(2):111-22. doi: 10.1016/0028-3908(88)90159-1.
Polygraphic 23-hr recordings were carried out in 25 adult cats in order to examine the effects of both systemic and local injections of various histaminergic and antihistaminergic drugs on sleep-waking cycles. alpha-Fluoromethylhistidine (alpha-FMH), a specific inhibitor of histidine decarboxylase, when injected intraperitoneally at a dose of 20 mg/kg, induced a significant increase in deep slow wave sleep (S2) and a decrease in wakefulness (W), without modifying light slow wave sleep (S1) and paradoxical sleep (PS). Intraperitoneal injections of mepyramine (1 mg and 5 mg/kg), a well-known histamine H1-receptor antagonist, increased deep slow wave sleep and decreased wakefulness, as well as paradoxical sleep. Bilateral injections of alpha-FMH (50 micrograms/1 microliter) into the ventrolateral posterior hypothalamus, where histamine immunoreactive neurones have been recently identified, resulted in a significant decrease in wakefulness and increase in deep slow wave sleep. Similarly, injections of mepyramine (120 micrograms/1 microliter) in the same structures caused a significant decrease in wakefulness and an increase in deep slow wave and paradoxical sleep as well. In contrast, local injections of SKF-91488 (50 micrograms/1 microliter), a specific inhibitor of histamine-N-methyltransferase, led to a significant increase in wakefulness and decrease in both slow wave sleep (SWS) and paradoxical sleep. Injections of histamine, at doses of 5, 30 and 60 micrograms/1 microliter, also increased wakefulness and decreased slow wave sleep dose dependently, while these effects were completely blocked by pretreatment with mepyramine. The results suggest that histaminergic systems in the hypothalamus play an important role in arousal mechanisms and their actions are mediated through H1-receptors.
为了研究全身和局部注射各种组胺能和抗组胺能药物对睡眠-觉醒周期的影响,对25只成年猫进行了23小时的多导记录。α-氟甲基组氨酸(α-FMH)是组氨酸脱羧酶的特异性抑制剂,当以20mg/kg的剂量腹腔注射时,可使深慢波睡眠(S2)显著增加,觉醒(W)减少,而不改变浅慢波睡眠(S1)和异相睡眠(PS)。腹腔注射著名的组胺H1受体拮抗剂美吡拉敏(1mg/kg和5mg/kg),可增加深慢波睡眠,减少觉醒以及异相睡眠。将α-FMH(50微克/1微升)双侧注射到最近已鉴定出组胺免疫反应性神经元的下丘脑腹后外侧,导致觉醒显著减少,深慢波睡眠增加。同样,在相同结构中注射美吡拉敏(120微克/1微升)也会导致觉醒显著减少,深慢波睡眠和异相睡眠增加。相反,局部注射组胺-N-甲基转移酶的特异性抑制剂SKF-91488(50微克/1微升),会导致觉醒显著增加,慢波睡眠(SWS)和异相睡眠减少。分别以5、30和60微克/1微升的剂量注射组胺,也会剂量依赖性地增加觉醒并减少慢波睡眠,而这些作用可被美吡拉敏预处理完全阻断。结果表明,下丘脑的组胺能系统在觉醒机制中起重要作用,其作用通过H1受体介导。