• Olivera Nesic, Julieann Lee, Kathia M Johnson, Zaiming Ye, Guo-Ying Xu, Geda C Unabia, Thomas G Wood, David J McAdoo, Karin N Westlund, Claire E Hulsebosch, and Regino Perez-Polo J J.
• Department of Human Biological Chemistry and Genetics, University of Texas Medical Branch, Galveston, Texas 77555-1072, USA.
• J. Neurochem. 2005 Nov 1; 95 (4): 998-1014.

AbstractCentral neuropathic pain (CNP) is an important problem following spinal cord injury (SCI), because it severely affects the quality of life of SCI patients. As in the patient population, the majority of rats develop significant allodynia (CNP rats) after moderate SCI. However, about 10% of SCI rats do not develop allodynia, or develop significantly less allodynia than CNP rats (non-CNP rats). To identify transcriptional changes underlying CNP development after SCI, we used Affymetrix DNA microarrays and RNAs extracted from the spinal cords of CNP and non-CNP rats. DNA microarry analysis showed significantly increased expression of a number of genes associated with inflammation and astrocytic activation in the spinal cords of rats that developed CNP. For example, mRNA levels of glial fibrilary acidic protein (GFAP) and Aquaporin 4 (AQP4) significantly increased in CNP rats. We also found that GFAP, S100beta and AQP4 protein elevation persisted for at least 9 months throughout contused spinal cords, consistent with the chronic nature of CNP. Thus, we hypothesize that CNP development results, in part, from dysfunctional, chronically "over-activated" astrocytes. Although, it has been shown that activated astrocytes are associated with peripheral neuropathic pain, this has not previously been demonstrated in CNP after SCI.

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