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发育期接触酒精会减少成年雄性大鼠的睡眠时间并损害其睡眠起始。

Reduced sleep and impaired sleep initiation in adult male rats exposed to alcohol during early postnatal period.

机构信息

Department of Animal Biology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.

出版信息

Behav Brain Res. 2012 Sep 1;234(1):38-42. doi: 10.1016/j.bbr.2012.06.002. Epub 2012 Jun 12.

DOI:10.1016/j.bbr.2012.06.002
PMID:22698707
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3412616/
Abstract

Prenatal alcohol exposure (AE) is associated with cognitive and neurobehavioral abnormalities, such as increased motor activity and elevated anxiety, that may last a lifetime. Persistent sleep disruption may underlie these problems. Using a rat model, we investigated long-term alterations of sleep-wake behavior following AE during a critical early developmental period. Male rats received 2.6 g/kg of alcohol intragastrically twice daily on postnatal days (PD) 4-9, a developmental period equivalent to the third trimester of human pregnancy (AE group), or were sham-intubated (S group). On PD52-80, they were instrumented for tethered electroencephalogram and nuchal electromyogram recording and habituated to the recording procedures. Sleep-wake behavior was then recorded during one 24 h-long session. Wake, slow-wave sleep (SWS) and rapid eye movement sleep (REMS) were scored in 10 s epochs during 6h of the lights-on (rest) and 6h of the lights-off (active) periods. During the active period, REMS percentage was significantly lower (4.7 ± 0.9 (SE) vs. 8.2 ± 0.9; p < 0.02) and the percentage of SWS tended to be lower (p = 0.07) in AE than S rats (N = 6/group). During the rest period, sleep and wake amounts did not differ between the groups, but AE rats had longer latency to both SWS and REMS onset (p = 0.02 and 0.003, respectively). Our data demonstrate that, in a rat model of prenatal AE, impaired sleep-wake behavior persists into the adulthood. Disordered sleep may exacerbate cognitive and behavioral disorders seen in human victims of prenatal AE.

摘要

产前酒精暴露(AE)与认知和神经行为异常有关,例如增加的运动活动和焦虑升高,这些异常可能持续一生。持续的睡眠中断可能是这些问题的基础。我们使用大鼠模型研究了在关键的早期发育期间,AE 后长期睡眠-觉醒行为的变化。雄性大鼠在出生后第 4-9 天(PD)每天两次通过胃内给予 2.6 g/kg 的酒精,这一发育时期相当于人类妊娠的第三个 trimester(AE 组),或进行假插管(S 组)。在 PD52-80,他们被安置用于固定脑电图和颈部肌电图记录,并适应记录程序。然后在一个 24 小时的长会话中记录睡眠-觉醒行为。在灯光开启(休息)的 6 小时和灯光关闭(活跃)的 6 小时期间,以 10 秒的时间段记录觉醒、慢波睡眠(SWS)和快速眼动睡眠(REMS)。在活跃期,AE 大鼠的 REMS 百分比明显降低(4.7 ± 0.9(SE)比 8.2 ± 0.9;p < 0.02),SWS 的百分比也倾向于降低(p = 0.07)(N = 6/组)。在休息期,两组之间的睡眠和觉醒量没有差异,但 AE 大鼠的 SWS 和 REMS 起始潜伏期更长(分别为 p = 0.02 和 0.003)。我们的数据表明,在产前 AE 的大鼠模型中,睡眠-觉醒行为障碍持续到成年期。睡眠障碍可能会加重人类产前 AE 受害者的认知和行为障碍。

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