Pain is the hallmark of patients with chronic prostatitis (CP) and chronic pelvic pain syndrome (CPPS). Despite numerous hypotheses the etiology and pathogenesis remain unknown. To better understand CP/CPPS we used a murine experimental autoimmune prostatitis (EAP) model to examine the development, localization and modulation of pelvic pain. Pelvic pain was detected 5 days after antigen instillation and was sustained beyond 30 days, indicating the development of chronic pain. The pain was attenuated by lidocaine treatment into the prostate, but not into the bladder or the colon suggesting that pain originated from the prostate. EAP histopathology was confined to the prostate with focal periglandular inflammatory infiltrates in the ventral, dorso-lateral and anterior lobes of the mouse prostate. Inflammation and pelvic pain were positively correlated and increased with time. Morphologically, the dorso-lateral prostate alone showed significantly increased neuronal fiber distribution as evidenced by increased PGP 9.5 expression. Pelvic pain was attenuated by treatment with the neuromodulator gabapentin, suggesting spinal and/or supraspinal contribution to chronic pain. These results provide the basis for identifying mechanisms that regulate pelvic pain and the testing of therapeutic agents that block pain development in CP/CPPS.