Background Prostatodynia remains a difficult clinical problem.Resiniferatoxin(RTX),an ultrapotent vanilloid,canproduce a selective and long-lasting desensitization of nociception via C-fiber sensory neurons.Substance P (SP) andcalcitonin gene-related peptide(CGRP)released from C-fibers are key neurotransmitters in visceral pain.In this study,we evaluated the analgesic effect of intrathecal RTX on rat prostatodynia.Methods Male Sprague-Dawley rats were divided into 3 groups for different treatment.In group A,sham operation waspreformed.In group B,100 μl complete Freund’s adjuvant(CFA)was injected into the rat’s bilateral ventral prostate toinduce chronic inflammation.In group C,after prostatitis formed,50 μl 10 nmol/L RTX was injected into the rat’slumbosacral (L5-S2) vertebral canal.SP and CGRP contents in the spinal cord were investigated byimmunohistochemistry and radioimmunoassay(RIA).Their transcriptional levels in dorsal root ganglion(DRG)weredetermined by reverse transcriptase polymerase chain reaction(RT-PCR).In addition,pelvic nerve afferent dischargewas recorded to explore the neuro-electrophysiological mechanisms underlying RTX-induced effect.Results SP and CGRP released in the spinal cord and their synthesis in DRG were increased significantly in responseto CFA-induced chronic prostatitis,whereas this increase was effectively inhibited by intrathecal RTX.Meanwhile,pelvicnerve afferent electrical activity was enhanced significantly in rats with chronic prostatitis,but it was attenuated markedlyin RTX-treated rats paralleled by the change of neuropeptides.Conclusions Intrathecal RTX administration could produce an analgesic effect on rat prostatodynia.Suppression ofpelvic nerve afferent electrical activity may be a crucial mechanism underlying RTX-induced analgesia.RTX intrathecalapplication may present a novel analgesic strategy of prostatodynia. Background Prostatodynia remains a difficult clinical problem. Resiniferatoxin (RTX), an ultrapotent vanilloid, canproduce a selective and long-lasting desensitization of nociception via C-fiber sensory neurons. Substance P (SP) and calcitonin gene-related peptide (CGRP) released from C -fibers are key neurotransmitters in visceral pain.In this study, we evaluated the analgesic effect of intrathecal RTX on rat prostatodynia. Methods Male Sprague-Dawley rats were divided into 3 groups for different treatment.In group A, sham operation waspreformed.In group B, 100 μl complete Freund’s adjuvant (CFA) was injected into the rat’s bilateral ventral prostate toinduce chronic inflammation. In group C, after prostatitis formed, 50 μl 10 nmol / L RTX was injected into the rat’s slumbacacral (L5-S2) vertebral canal. SP and CGRP contents in the spinal cord were investigated by immunohistochemistry and radioimmunoassay (RIA). Their transcriptional levels in dorsal root ganglion (DRG) weredetermined by reverse transcriptase In addition, pelvic nerve afferent discharge was recorded to explore the neuro-electrophysiological mechanisms underlying RTX-induced effect. Results SP and CGRP released in the spinal cord and their synthesis in DRG were increased significantly in response to CFA -induced chronic prostatitis, and this increase was actually inhibited by intrathecal RTX.Meanwhile, pelvic nerves afferent electrical activity was enhanced significantly in rats with chronic prostatitis, but it was attenuated markedly in RTX-treated rats paralleled by the change of neuropeptides. Conclusions Intrathecal RTX administration could produce an analgesic effect on rat prostatodynia. Supression ofpelvic nerve afferent electrical activity may be a crucial mechanism underlying RTX-induced analgesia. RTX intrathecalapplication may present a novel analgesic strategy of prostatodynia.