Gonzalez M M, Debilly G, Valatx J L, Jouvet M
Département de Médecine Expérimentale, Université Claude Bernard, INSERM U52, CNRS UA1195, Lyon, France.
Neurosci Lett. 1995 Dec 29;202(1-2):5-8. doi: 10.1016/0304-3940(95)12209-5.
In a preliminary study we showed that the sleep rebound occurring after sleep deprivation is decreased in rats treated with N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP-4), a neurotoxic agent specific for the noradrenergic cells of the locus coeruleus (LC). Sleep deprivation methods not only involve sleep loss, but also stress, which per se may induce an increase in sleep duration. Extensive research showed that the locus coeruleus is involved in stress. To evaluate the participation of LC in this mechanism, the effect of DSP-4 treatment was studied on sleep duration following a short intense stress in the absence of sleep loss. The results showed that the augmentation of sleep after 1 h of immobilization stress is lower in DSP-4-treated rats (slow-wave sleep duration, -24%; paradoxical sleep duration, -52%). These findings suggest that the increase in sleep induced by such a stressor is mediated, at least in part, by the noradrenergic LC.
在一项初步研究中,我们发现,用N-(2-氯乙基)-N-乙基-2-溴苄胺(DSP-4)处理的大鼠,在睡眠剥夺后出现的睡眠反弹减少,DSP-4是一种对蓝斑(LC)去甲肾上腺素能细胞具有特异性的神经毒性剂。睡眠剥夺方法不仅涉及睡眠缺失,还涉及应激,应激本身可能会导致睡眠时间增加。广泛的研究表明,蓝斑参与了应激反应。为了评估LC在这一机制中的作用,我们研究了DSP-4处理对在无睡眠缺失情况下短时间强烈应激后睡眠时间的影响。结果表明,在经DSP-4处理的大鼠中,固定应激1小时后的睡眠增加幅度较小(慢波睡眠时间,-24%;异相睡眠时间,-52%)。这些发现表明,这种应激源诱导的睡眠增加至少部分是由去甲肾上腺素能LC介导的。