Spinal cord injury induces early and persistent lesional P2X4 receptor expression
Spinal cord injury induces early and persistent lesional P2X4 receptor expression
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DOI：
10.1016/j.jneuroim.2005.02.016
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发表时间：
2005-06-01
影响因子：
3.3
通讯作者：
Schluesener, HJ
中科院分区：
文献类型：
--
作者：
Schwab, JM;Guo, LH;Schluesener, HJ
脊髓损伤（SCI）后，神经性慢性疼痛是残疾的主要原因。最近，胶质细胞P2 X（4）受体（P2 X（4）R）已被确定为周围神经损伤后神经病理性疼痛的主要贡献者。在这里，我们报告了大鼠SCI后P2 X（4）R表达的分析。P2 X（4）R（+）细胞的显著损伤积累早在SCI后24小时就被检测到，在第7天达到最大细胞数量。此后，细胞数量下降，但持续在显著升高的次最大水平（>70%），直到损伤后1个月。双重免疫标记鉴定了大部分损伤的P2 X（4）R（+）细胞为活化的小胶质细胞/巨噬细胞和存活的神经元/神经突。P2 X（4）R（+）、β-APP（+）肥大神经突的增加与病变的接近程度相关。此外，P2 X（4）R（+）细胞共表达信号级联的细胞内调节因子，考克斯-1（>20%）、考克斯-2（>5%）、RhoA（>60%）和RhoB（>10%）。(C)2005 Elsevier B. V.保留所有权利。
Following spinal cord injury (SCI), neuropathic, chronic pain is a major cause of disability. Recently, glial P2X(4) receptor (P2X(4)R) has been identified as a major contributor to the development of neuropathic pain after peripherial nerve injury. Here we report analysis of P2X(4)R expression following rat SCI. Significant lesional accumulation of P2X(4)R(+) cells was detected as early as 24 It after SCI, reaching maximum cell numbers on Day 7. Thereafter cell numbers declined but persisted at significantly elevated, sub-maximal levels (>70%) until 1 month post injury. Double-immunolabeling identified the majority of lesional P2X(4)R(+) cells as activated microglia/rnacrophages and surviving neurons/neurites. Increase of P2X(4)R(+), beta-APP(+) hypertrophic neurites correlated with proximity to the lesion. Further, P2X(4)R(+) cells coexpressed the intracellular regulators of signalling cascades, COX-1 (>20%), COX-2 (>5%), RhoA (>60%) and RhoB (>10%). (C) 2005 Elsevier B.V. All rights reserved.