Up-regulation of spinal microglial Iba-1 expression persists after resolution of neuropathic pain hypersensitivity

被引:28
|
作者
Leinders, Mathias [1 ,2 ]
Knaepen, Liesbeth [1 ]
De Kock, Marc [3 ]
Sommer, Claudia [2 ]
Hermans, Emmanuel [1 ]
Deumens, Ronald [1 ]
机构
[1] Catholic Univ Louvain, Grp Neuropharmacol, Inst Neurosci, B-1200 Brussels, Belgium
[2] Univ Wurzburg, Dept Neurol, D-97080 Wurzburg, Germany
[3] UCL Med Sch, St Luc Hosp, Dept Anesthesiol, B-1200 Brussels, Belgium
关键词
Inflammation; Nerve injury; Rat; Spinal cord; Pain mechanisms; PERIPHERAL-NERVE INJURY; MECHANICAL ALLODYNIA; INFLAMMATORY PAIN; TACTILE ALLODYNIA; GFAP EXPRESSION; GLIA; PREVENTION; INSIGHTS; SYSTEM; MODEL;
D O I
10.1016/j.neulet.2013.08.062
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Spinal microglial activation plays a major role in the development of neuropathic pain following peripheral nerve injury. We here provide evidence for an elevated expression of the microglial marker Iba-1 in the lumbar dorsal horn ipsilateral to L5 spinal nerve transection that persists for at least 14 weeks, a time at which mechanical hypersensitivity had fully resolved. Iba-1 expression was, however; significantly lower than at 4 weeks. We therefore conclude that microglia remain partly activated beyond the phase of pain hypersensitivity. Thus, the relation between microglial cells and neuropathic pain outcome is subject to change over time after nerve injury. (C) 2013 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:146 / 150
页数:5
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