Thus, the results of this study support the hypothesis that the release of pro-inflammatory mediators, probably TNF-α, during acute colitis contributes to the up-regulation of P2X3 receptors causing hyperexcitability in small-diameter DRG neurons innervating the inflamed colon, which may lead to nociceptive signals in the central nervous system (CNS) and contribute at least in part to nociceptive plasticity of visceral afferents. The gene discussed is TNF; the disease is colitis.