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吉兰-巴雷综合征模型中与机械性超敏反应相关的脊柱变化。

Spinal changes associated with mechanical hypersensitivity in a model of Guillain-Barré syndrome.

作者信息

Luongo Livio, Sajic Marija, Grist John, Clark Anna K, Maione Sabatino, Malcangio Marzia

机构信息

Neurorestoration group, Wolfson Centre for Age Related Diseases, King's College London, London, UK.

出版信息

Neurosci Lett. 2008 May 30;437(2):98-102. doi: 10.1016/j.neulet.2008.04.019. Epub 2008 Apr 10.

DOI:10.1016/j.neulet.2008.04.019
PMID:18448252
Abstract

Guillain-Barré syndrome (GBS) is an inflammatory disease of the peripheral nervous system which can cause pain via mechanisms that are poorly understood. Here, we show that in rat experimental autoimmune neuritis (EAN) mechanical allodynia developed up to 9 days before the onset of detectable neurological deficits. Allodynia was associated with an increase in the number of microglial cells in the dorsal horn of the spinal cord. The expression of the chemokine CX3CL1 (fractalkine) and its receptor CX3CR1 were also higher in EAN than in control dorsal horns suggesting spinal microglia and CX3CL1/CX3CR1 may play a role in the pain-like behaviour.

摘要

吉兰-巴雷综合征(GBS)是一种外周神经系统的炎症性疾病,其通过尚不清楚的机制引发疼痛。在此,我们表明,在大鼠实验性自身免疫性神经炎(EAN)中,机械性异常性疼痛在可检测到的神经功能缺损出现前9天就已出现。异常性疼痛与脊髓背角小胶质细胞数量增加有关。趋化因子CX3CL1(fractalkine)及其受体CX3CR1在EAN中的表达也高于对照背角,提示脊髓小胶质细胞和CX3CL1/CX3CR1可能在类似疼痛行为中起作用。

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