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睡眠剥夺后通过 GABA 和乙酰胆碱毒蕈碱受体对运动三叉神经神经元进行的体内平衡调节。

Homeostatic regulation through GABA and acetylcholine muscarinic receptors of motor trigeminal neurons following sleep deprivation.

机构信息

Department of Neurology and Neurosurgery, McGill University, Montreal Neurological Institute, 3801 University Street, Montreal, QC, H3A 2B4, Canada.

出版信息

Brain Struct Funct. 2017 Sep;222(7):3163-3178. doi: 10.1007/s00429-017-1392-4. Epub 2017 Mar 15.

DOI:10.1007/s00429-017-1392-4
PMID:28299422
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5585289/
Abstract

Muscle tone is regulated across sleep-wake states, being maximal in waking, reduced in slow wave sleep (SWS) and absent in paradoxical or REM sleep (PS or REMS). Such changes in tone have been recorded in the masseter muscles and shown to correspond to changes in activity and polarization of the trigeminal motor 5 (Mo5) neurons. The muscle hypotonia and atonia during sleep depend in part on GABA acting upon both GABA and GABA receptors (Rs) and acetylcholine (ACh) acting upon muscarinic 2 (AChM2) Rs. Here, we examined whether Mo5 neurons undergo homeostatic regulation through changes in these inhibitory receptors following prolonged activity with enforced waking. By immunofluorescence, we assessed that the proportion of Mo5 neurons positively stained for GABARs was significantly higher after sleep deprivation (SD, ~65%) than sleep control (SC, ~32%) and that the luminance of the GABAR fluorescence was significantly higher after SD than SC and sleep recovery (SR). Although, all Mo5 neurons were positively stained for GABARs and AChM2Rs (100%) in all groups, the luminance of these receptors was significantly higher following SD as compared to SC and SR. We conclude that the density of GABA, GABA and AChM2 receptors increases on Mo5 neurons during SD. The increase in these receptors would be associated with increased inhibition in the presence of GABA and ACh and thus a homeostatic down-scaling in the excitability of the Mo5 neurons after prolonged waking and resulting increased susceptibility to muscle hypotonia or atonia along with sleep.

摘要

肌肉张力在睡眠-觉醒状态中调节,在觉醒时最大,在慢波睡眠(SWS)中减少,在反常或 REM 睡眠(PS 或 REMS)中消失。这种张力变化已在咀嚼肌中记录,并显示与三叉运动 5(Mo5)神经元的活动和极化变化相对应。睡眠期间的肌肉张力降低和弛缓部分依赖于 GABA 作用于 GABA 和 GABA 受体(Rs)以及乙酰胆碱(ACh)作用于毒蕈碱 2(AChM2)Rs。在这里,我们研究了 Mo5 神经元是否通过在长时间活动后这些抑制性受体的变化进行自身调节。通过免疫荧光,我们评估了 Mo5 神经元中 GABA Rs 阳性染色的比例在睡眠剥夺(SD,约 65%)后显著高于睡眠对照(SC,约 32%),并且 SD 后 GABA Rs 的荧光亮度显著高于 SC 和睡眠恢复(SR)。尽管在所有组中,所有 Mo5 神经元都被 GABA Rs 和 AChM2Rs(100%)阳性染色,但与 SC 和 SR 相比,SD 后这些受体的亮度显著增加。我们得出结论,在 SD 期间,Mo5 神经元上的 GABA、GABA 和 AChM2 受体密度增加。这些受体的增加将与 GABA 和 ACh 存在时的抑制增加相关,因此在长时间清醒后,Mo5 神经元的兴奋性会进行自身平衡下调,从而导致肌肉张力降低或弛缓,以及睡眠时增加对肌肉张力降低或弛缓的易感性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24a9/5585289/1a8c71b3cf63/429_2017_1392_Fig7_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24a9/5585289/9a4fc9f5165a/429_2017_1392_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24a9/5585289/1e5f0137e57f/429_2017_1392_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24a9/5585289/1a8c71b3cf63/429_2017_1392_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24a9/5585289/d05141e47111/429_2017_1392_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24a9/5585289/b80d9cbbfc1d/429_2017_1392_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24a9/5585289/9011ba97467a/429_2017_1392_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24a9/5585289/6516a44003ce/429_2017_1392_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24a9/5585289/9a4fc9f5165a/429_2017_1392_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24a9/5585289/1e5f0137e57f/429_2017_1392_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24a9/5585289/1a8c71b3cf63/429_2017_1392_Fig7_HTML.jpg

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