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

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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]

References

  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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