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慢性疲劳综合征模型通过脊髓小胶质细胞激活表现出机械性痛觉过敏和肌肉痛觉过敏。

A chronic fatigue syndrome model demonstrates mechanical allodynia and muscular hyperalgesia via spinal microglial activation.

机构信息

Department of Functional Anatomy and Neuroscience, Graduate School of Medicine, Nagoya University, Nagoya, Aichi, Japan; Core Research for Evolutional Science and Technology (CREST) of the Japan Science and Technology Agency, Saitama, Japan.

出版信息

Glia. 2014 Sep;62(9):1407-17. doi: 10.1002/glia.22687. Epub 2014 May 23.

Abstract

Patients with chronic fatigue syndrome (CFS) and fibromyalgia syndrome (FMS) display multiple symptoms, such as chronic widespread pain, fatigue, sleep disturbance, and cognitive dysfunction. Abnormal pain sensation may be the most serious of these symptoms; however, its pathophysiology remains unknown. To provide insights into the molecular basis underlying abnormal pain in CFS and FMS, we used a multiple continuous stress (CS) model in rats, which were housed in a cage with a low level of water (1.5 cm in depth). The von Frey and Randall-Seritto tests were used to evaluate pain levels. Results showed that mechanical allodynia at plantar skin and mechanical hyperalgesia at the anterior tibialis (i.e., muscle pain) were induced by CS loading. Moreover, no signs of inflammation and injury incidents were observed in both the plantar skin and leg muscles. However, microglial accumulation and activation were observed in L4-L6 dorsal horn of CS rats. Quantification analysis revealed a higher accumulation of microglia in the medial part of Layers I-IV of the dorsal horn. To evaluate an implication of microglia in pain, minocycline was intrathecally administrated (via an osmotic pump). Minocycline significantly attenuated CS-induced mechanical hyperalgesia and allodynia. These results indicated that activated microglia were involved in the development of abnormal pain in CS animals, suggesting that the pain observed in CFS and FMS patients may be partly caused by a mechanism in which microglial activation is involved.

摘要

慢性疲劳综合征(CFS)和纤维肌痛综合征(FMS)患者表现出多种症状,如慢性广泛性疼痛、疲劳、睡眠障碍和认知功能障碍。异常的疼痛感觉可能是这些症状中最严重的,但它的病理生理学仍然未知。为了深入了解 CFS 和 FMS 异常疼痛的分子基础,我们使用了一种多连续应激(CS)模型,将大鼠安置在一个水深为 1.5 厘米的低水位笼中。von Frey 和 Randall-Seritto 测试用于评估疼痛水平。结果表明,足底皮肤的机械性痛觉过敏和胫骨前肌的机械性痛觉过敏(即肌肉疼痛)是由 CS 加载引起的。此外,在足底皮肤和腿部肌肉中均未观察到炎症和损伤事件的迹象。然而,在 CS 大鼠的 L4-L6 背角观察到小胶质细胞的积累和激活。定量分析显示,背角 I-IV 层内侧部分的小胶质细胞积累更高。为了评估小胶质细胞在疼痛中的作用,鞘内给予米诺环素(通过渗透泵)。米诺环素显著减轻了 CS 诱导的机械性痛觉过敏和痛觉过敏。这些结果表明,激活的小胶质细胞参与了 CS 动物异常疼痛的发展,这表明 CFS 和 FMS 患者观察到的疼痛可能部分是由小胶质细胞激活参与的机制引起的。

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