Naftopidil is used clinically for the treatment of voiding disorders in benign prostatic hyperplasia. Previous in vivo studies in which naftopidil was applied intrathecally abolished rhythmic bladder contraction, suggesting that naftopidil might inhibit a voiding reflex through interaction with spinal dorsal horn neurons. In this study, we aimed to clarify the mechanism of action of naftopidil on spinal dorsal horn neurons by using patch-clamp recording of rat spinal cord slices. In about 30% of neurons, naftopidil increased the frequency of miniature inhibitory postsynaptic currents (mIPSCs) tested. These naftopidil activities were reversible and concentration-dependent manner, and interestingly, bath applied another alpha-1 adrenoceptor antagonist prazosin did not effects of mIPSCs. Although naftopidil was developed as an a-1 adrenoceptor antagonist, our previous studies showed that the activation of an alpha -1 adrenoceptor in substantia gelatinosa (SG) increases the frequency of mIPSCs. This result suggested that, under our conditions, naftopidil may interact with a site(s) in the spinal dorsal horn. These data suggest that naftopidil enhances the release of GABA and/or glycine by activating inhibitory interneuron terminals in the spinal dorsal horn via an unclear site(s) other than an alpha-1 adrenoceptor and thereby modulates sensory transmission in SG.