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Transcriptional profiling of spinal cord injury-induced central neuropathic pain.

Authors: Nesic, O  Lee, J  Johnson, KM  Ye, Z  Xu, GY  Unabia, GC  Wood, TG  McAdoo, DJ  Westlund, KN  Hulsebosch, CE  Regino Perez-Polo, J 
Citation: Nesic O, etal., J Neurochem. 2005 Nov;95(4):998-1014. Epub 2005 Oct 10.
Pubmed: (View Article at PubMed) PMID:16219025
DOI: Full-text: DOI:10.1111/j.1471-4159.2005.03462.x

Central 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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RGD ID: 8695957
Created: 2014-08-07
Species: All species
Last Modified: 2014-08-07
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.