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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Spinal cord injury induces early and persistent lesional P2X4 receptor expression.

Following spinal cord injury (SCI), neuropathic, chronic pain is a major cause of disability. Recently, glial P2X4 receptor (P2X4R) has been identified as a major contributor to the development of neuropathic pain after peripheral nerve injury. Here we report analysis of P2X4R expression following rat SCI. Significant lesional accumulation of P2X4R+ cells was detected as early as 24 h 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 P2X4R+ cells as activated microglia/macrophages and surviving neurons/neurites. Increase of P2X4R+, beta-APP+ hypertrophic neurites correlated with proximity to the lesion. Further, P2X4R+ cells coexpressed the intracellular regulators of signalling cascades, COX-1 (>20%), COX-2 (>5%), RhoA (>60%) and RhoB (>10%).[1]


  1. Spinal cord injury induces early and persistent lesional P2X4 receptor expression. Schwab, J.M., Guo, L., Schluesener, H.J. J. Neuroimmunol. (2005) [Pubmed]
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