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异相睡眠剥夺期间的慢性应激会增加异相睡眠反弹:与血浆催乳素水平和脑血清素含量的关联

Chronic stress during paradoxical sleep deprivation increases paradoxical sleep rebound: association with prolactin plasma levels and brain serotonin content.

作者信息

Machado Ricardo Borges, Tufik Sergio, Suchecki Deborah

机构信息

Department of Psychobiology, Universidade Federal de São Paulo, São Paulo, Brazil.

出版信息

Psychoneuroendocrinology. 2008 Oct;33(9):1211-24. doi: 10.1016/j.psyneuen.2008.06.007.

Abstract

Previous studies suggest that stress associated to sleep deprivation methods can affect the expression of sleep rebound. In order to examine this association and possible mechanisms, rats were exposed to footshock stress during or immediately after a 96-h period of paradoxical sleep deprivation (PSD) and their sleep and heart rate were recorded. Control rats (maintained in individual home cages) and paradoxical sleep-deprived (PS-deprived) rats were distributed in three conditions (1) no footshock--NF; (2) single footshock--SFS: one single footshock session at the end of the PSD period (6-8 shocks per minute; 100 ms; 2 mA; for 40 min); and (3) multiple footshock--MFS: footshock sessions with the same characteristics as described above, twice a day throughout PSD (at 7:00 h and 19:00 h) and one extra session before the recovery period. After PSD, animals were allowed to sleep freely for 72 h. Additional groups were sacrificed at the end of the sleep deprivation period for blood sampling (ACTH, corticosterone, prolactin and catecholamine levels) and brain harvesting (monoamines and metabolites). Neither SFS nor MFS produced significant alterations in the sleep patterns of control rats. All PS-deprived groups exhibited increased heart rate which could be explained by increased dopaminergic activity in the medulla. As expected, PS deprivation induced rebound of paradoxical sleep in the first day of recovery; however, PSD+MFS group showed the highest rebound (327.3% above the baseline). This group also showed intermediate levels of corticosterone and the highest levels of prolactin, which were positively correlated with the length of PS episodes. Moreover, paradoxical sleep deprivation resulted in elevation of the serotonergic turnover in the hypothalamus, which partly explained the hormonal results, and in the hippocampus, which appears to be related to adaptive responses to stress. The data are discussed in the realm of a prospective importance of paradoxical sleep for processing of traumatic events.

摘要

先前的研究表明,与睡眠剥夺方法相关的压力会影响睡眠反弹的表现。为了研究这种关联及可能的机制,在96小时异相睡眠剥夺(PSD)期间或之后,让大鼠遭受足部电击应激,并记录它们的睡眠和心率。将对照大鼠(饲养在单独的饲养笼中)和异相睡眠剥夺(PS剥夺)大鼠分为三种情况:(1)无足部电击——NF;(2)单次足部电击——SFS:在PSD期结束时进行一次单次足部电击(每分钟6 - 8次电击;100毫秒;2毫安;持续40分钟);(3)多次足部电击——MFS:在整个PSD期间每天两次进行与上述相同特征的足部电击(上午7:00和下午19:00),并在恢复期前额外进行一次。PSD后,让动物自由睡眠72小时。在睡眠剥夺期结束时,处死额外的几组动物以进行血液采样(促肾上腺皮质激素、皮质酮、催乳素和儿茶酚胺水平)和脑采集(单胺和代谢产物)。SFS和MFS对对照大鼠的睡眠模式均未产生显著改变。所有PS剥夺组的心率均升高,这可以通过延髓中多巴胺能活性增加来解释。正如预期的那样,PS剥夺在恢复的第一天诱导了异相睡眠的反弹;然而,PSD + MFS组的反弹最高(比基线高327.3%)。该组的皮质酮水平也处于中等水平,催乳素水平最高,且与PS发作时长呈正相关。此外,异相睡眠剥夺导致下丘脑5-羟色胺能周转率升高,这部分解释了激素结果,同时海马体中的5-羟色胺能周转率也升高,这似乎与对应激的适应性反应有关。本文在异相睡眠对创伤事件处理的潜在重要性这一领域对数据进行了讨论。

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