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神经病理性疼痛诱导的睡眠障碍模型大鼠褪黑素分泌的变化

Changes of melatonin secretion in the neuropathic pain induced sleep disorder model rat.

作者信息

Fujimoto Moe, Sekiyama Hiroshi, Nakamoto Hirofumi, Takata Junko, Sawamura Shigehito

机构信息

Department of Anesthesiology, Teikyo University School of Medicine, Kaga 2-11-1, Itabashi-Ku, Tokyo, 173-8605 Japan.

出版信息

Sleep Biol Rhythms. 2024 May 31;22(4):463-470. doi: 10.1007/s41105-024-00529-w. eCollection 2024 Oct.

DOI:10.1007/s41105-024-00529-w
PMID:39300980
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11408445/
Abstract

Chronic pain due to peripheral neuropathy can lead to sleep disorders that significantly worsen the patient's quality of life. Previously, we conducted brain wave measurements in a rat model of neuropathic pain and identified its potential as a model for sleep disorders associated with chronic pain (reported). In this study, we quantified melatonin secretion and assessed its circadian rhythm in a rat model of pain-induced sleep disorder. To create a model of chronic constriction injury (CCI), rats were loosely tied around the sciatic nerve, with approximately 1 mm spacing, 14 days before the experiment. Rats with no ties around the sciatic nerve were used as controls. Electroencephalograms and electromyograms were recorded for 3 days, and the episodes of waking, REM sleep, and non-REM sleep were compared between the groups. The samples for microanalysis were collected every 30 min and used for melatonin analysis. Compared to the control group, the CCI model group exhibited an increase in wake episodes and a decrease in non-REM sleep episodes. Analysis of the area under the curve of melatonin secretion revealed a significant increase in melatonin secretion and a loss of circadian rhythm in the CCI model group. Melatonin secretion markedly increased accompanied by loss of circadian rhythm in a rat model of CCI. Further studies investigating the causal relationship between neuropathic pain and melatonin secretion are warranted.

摘要

外周神经病变所致的慢性疼痛可导致睡眠障碍,显著恶化患者的生活质量。此前,我们在神经性疼痛大鼠模型中进行了脑电波测量,并确定其作为与慢性疼痛相关的睡眠障碍模型的潜力(已报道)。在本研究中,我们在疼痛诱导的睡眠障碍大鼠模型中量化了褪黑素分泌,并评估了其昼夜节律。为建立慢性缩窄性损伤(CCI)模型,在实验前14天,将大鼠坐骨神经周围松散结扎,间距约1毫米。坐骨神经未结扎的大鼠用作对照。记录脑电图和肌电图3天,并比较两组之间的清醒、快速眼动睡眠和非快速眼动睡眠发作情况。每30分钟采集一次用于微量分析的样本,并用于褪黑素分析。与对照组相比,CCI模型组的清醒发作增加,非快速眼动睡眠发作减少。对褪黑素分泌曲线下面积的分析显示,CCI模型组褪黑素分泌显著增加,昼夜节律丧失。在CCI大鼠模型中,褪黑素分泌显著增加,同时昼夜节律丧失。有必要进一步研究神经性疼痛与褪黑素分泌之间的因果关系。