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脑催乳素参与应激诱导的快速眼动睡眠反弹。

Brain prolactin is involved in stress-induced REM sleep rebound.

作者信息

Machado Ricardo Borges, Rocha Murilo Ramos, Suchecki Deborah

机构信息

Universidade Ibirapuera, Psychosomatic Research Group, Department of Psychology, Brazil; Universidade Ibirapuera, Department of Pharmacy, Brazil.

Department of Psychobiology, Escola Paulista de Medicina, Universidade Federal de São Paulo, Brazil.

出版信息

Horm Behav. 2017 Mar;89:38-47. doi: 10.1016/j.yhbeh.2016.12.004. Epub 2016 Dec 23.

DOI:10.1016/j.yhbeh.2016.12.004
PMID:28017595
Abstract

REM sleep rebound is a common behavioural response to some stressors and represents an adaptive coping strategy. Animals submitted to multiple, intermittent, footshock stress (FS) sessions during 96h of REM sleep deprivation (REMSD) display increased REM sleep rebound (when compared to the only REMSD ones, without FS), which is correlated to high plasma prolactin levels. To investigate whether brain prolactin plays a role in stress-induced REM sleep rebound two experiments were carried out. In experiment 1, rats were either not sleep-deprived (NSD) or submitted to 96h of REMSD associated or not to FS and brains were evaluated for PRL immunoreactivity (PRL-ir) and determination of PRL concentrations in the lateral hypothalamus and dorsal raphe nucleus. In experiment 2, rats were implanted with cannulas in the dorsal raphe nucleus for prolactin infusion and were sleep-recorded. REMSD associated with FS increased PRL-ir and content in the lateral hypothalamus and all manipulations increased prolactin content in the dorsal raphe nucleus compared to the NSD group. Prolactin infusion in the dorsal raphe nucleus increased the time and length of REM sleep episodes 3h after the infusion until the end of the light phase of the day cycle. Based on these results we concluded that brain prolactin is a major mediator of stress-induced REMS. The effect of PRL infusion in the dorsal raphe nucleus is discussed in light of the existence of a bidirectional relationship between this hormone and serotonin as regulators of stress-induced REM sleep rebound.

摘要

快速眼动睡眠反弹是对某些应激源的常见行为反应,代表一种适应性应对策略。在96小时快速眼动睡眠剥夺(REMSD)期间接受多次间歇性足部电击应激(FS)的动物,与仅接受REMSD而无FS的动物相比,表现出增强的快速眼动睡眠反弹,这与高血浆催乳素水平相关。为了研究脑内催乳素是否在应激诱导的快速眼动睡眠反弹中起作用,进行了两项实验。在实验1中,大鼠要么不进行睡眠剥夺(NSD),要么接受96小时的REMSD,有无FS,对大脑进行催乳素免疫反应性(PRL-ir)评估,并测定下丘脑外侧和中缝背核中的催乳素浓度。在实验2中,给大鼠在中缝背核植入插管用于催乳素输注,并记录睡眠情况。与FS相关的REMSD增加了下丘脑外侧的PRL-ir和含量,与NSD组相比,所有操作都增加了中缝背核中的催乳素含量。在中缝背核输注催乳素增加了输注后3小时直至日周期光期结束时快速眼动睡眠发作的时间和长度。基于这些结果,我们得出结论,脑内催乳素是应激诱导的快速眼动睡眠的主要调节因子。根据这种激素与作为应激诱导的快速眼动睡眠反弹调节因子的血清素之间存在双向关系,讨论了在中缝背核输注PRL的作用。

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