Current therapy for inflammatory pain includes selective opioid receptor agonists. Activation of opioid receptors lead to the modulation of voltage-gated ion channels, but it is unclear if opioids can also modulate ligand gated ion channel transient receptor potential vanilloid type 1 (TRPV1). TRPV1 channels are involved in thermosensation and are mainly expressed in peripheral nociceptive neurons, participating in the transduction of peripheral noxious stimuli. The present study examined whether TRPV1 activity can be modulated by opioids in dorsal root ganglion (DRG) neurons from rats with and without hindpaw inflammation. In whole-cell patch clamp studies morphine and DAMGO significantly decreased capsaicin-induced TRPV1 currents in DRG neurons in a naloxone reversible manner. The opioid-induced inhibition of TRPV1 currents was blunted by pertussis toxin. We could show that the effect of morphine on TRPV1 could be abolished by forskolin, indicating a potential role of cAMP/PKA pathway. In summary, our results indicate that opioid receptors can interfere with TRPV1 activity by activation of inhibitory G-proteins mediated by cAMP/PKA. This interaction describes a new molecular target for opioids to inhibit inflammatory pain.