Studies in animals have demonstrated mechanical and thermal hyperalgesia after systemic or local injection of the pro-inflammatory cytokines TNFa or IL-1b. Because the TRPV1 receptor is essential for the development of inflammatory thermal hyperalgesia we investigated if TNFa or IL-1ß influences TRPV1 receptor expression in cultured DRG neurons. DRG neurons were removed from normal rats, normal mice or from knockout mice (TNFR1-/-, TNFR2-/-, TNFR1/R2-/-) and cultured overnight. TNFa (0.6 nM or 3 nM) or IL-1ß (1nM or 1mM) was repetitively added to the cultures for two days. Antibodies against TRPV1, TNFR1, -R2 and IL-1R1 receptors were used to determine receptor expression. We found that 27.7%± 10.7% of all DRG neurons from rat express the TNFR1, 57.7%± 9.4% the TNFR2 and part of DRG neurons express IL-R1. When IL-1ß was added to the cultures for two days the expression of the TRPV1 was not changed. But after TNFa treatment (0.6 nM or 3 nM) 55.5%±7.8 resp. 66.25%± 8.46% of the neurons showed TRPV1-li IR (versus 34.5%± 2.5% in untreated neurons). This up-regulation failed in TNFR1/R2-/- and in TNFR1-/- mice but not in TNFR2-/-mice. We conclude that the expression of the TRPV1 receptor in DRG neurons of rat and mice can be influenced by TNFaprobable via the activation of the TNFR1 receptor.