Involvement of presynaptic TRPV1 channels in prostaglandin E-induced facilitation of spontaneous synaptic transmission in the rat spinal trigeminal subnucleus caudalis.

Prostaglandin E (PGE) synthesized in the central nervous system influences various physiological functions including nociception. Recently, we have demonstrated that PGE facilitates spontaneous synaptic transmission through presynaptic EP1 receptors in the spinal trigeminal subnucleus caudalis (Vc) neurons that receive nociceptive signals from the orofacial area. Increasing evidence suggests that the action of PGE is related to activation of transient receptor potential vanilloid 1 (TRPV1) channels. The present study investigated whether TRPV1 channels contribute to the facilitatory effect of PGE on synaptic transmission in the Vc neurons. Spontaneous excitatory and inhibitory postsynaptic currents (sEPSCs and sIPSCs) were recorded from Vc neurons in the rat brainstem slice by whole-cell patch-clamp mode. Superfusion of capsaicin (0.3, 1.0 μM) concentration-dependently increased the frequency of both sEPSCs and sIPSCs without any significant effect on their amplitude. The effect of capsaicin was completely abolished by a TRPV1 channel blocker AMG9810 (0.1 μM). PGE (5.0 μM) increased the frequency of sEPSCs and sIPSCs. This facilitatory effect of PGE was attenuated by AMG9810 and in neurons desensitized by repeated application of capsaicin. While a low concentration of either PGE (1.0 μM) or capsaicin (0.1 μM) had an insignificant effect on the sEPSCs and sIPSCs, co-application of these drugs increased their frequency. The present study demonstrated involvement of the presynaptic TRPV1 channels in PGE-induced facilitation of spontaneous synaptic transmissions and suggests interaction of PGE with TRPV1 channels in modification of nociceptive signals from the orofacial area to the Vc neurons.