Peripheral inflammatory and
neuropathic pain are closely related to the activation of
purinergic receptor P2X ligand-gated ion channel 3 (P2X3) and transient receptor potential vanilloid 1 (TRPV1), but the interaction between P2X3 and TRPV1 in different types of pathological
pain has rarely been reported. In this study, complete
Freund's adjuvant (CFA)-induced inflammatory
pain and spared nerve injury (SNI)-induced
neuropathic pain models were established in adult rats. The interactions between P2X3 and TRPV1 in the dorsal root ganglion were observed by pharmacological, co-immunoprecipitation, immunofluorescence and whole-cell patch-clamp recording assays. TRPV1 was shown to promote the induction of spontaneous
pain caused by P2X3 in the SNI model, but the induction of spontaneous
pain behaviour by TRPV1 was not completely dependent on P2X3 in vivo. In both the CFA and SNI models, the activation of peripheral P2X3 enhanced the effect of TRPV1 on spontaneous
pain, while the inhibition of peripheral TRPV1 reduced the induction of spontaneous
pain by P2X3 in the CFA model. TRPV1 and P2X3 had inhibitory effects on each other in the inflammatory
pain model. During
neuropathic pain, P2X3 facilitated the function of TRPV1, while TRPV1 had an inhibitory effect on P2X3. These results suggest that the mutual effects of P2X3 and TRPV1 differ in cases of inflammatory and
neuropathic pain in rats.