Quantitative real time-PCR was used to test whether cavernous nerve injury leads to a decrease in major pelvic ganglia (MPG) neuronal nicotinic acetylcholine receptor (nAChR) subunit and postsynaptic density-93 (PSD-93) transcript levels. Subunits α3, β4 and α7, commonly expressed in MPG, were selected for analysis. After 72 hours in explant culture, MPG transcript levels for α3, β4, α7, and PSD-93 were depressed significantly. Three days following cavernous nerve axotomy or crush in vivo, transcript levels for α3, β4 and PSD-93, but not for α7, were significantly depressed. Three days after dissecting the cavernous nerve free of underlying tissue and applying a 5 mm lateral stretch (manipulation), the transcript levels for α3 and PSD-93 also were decreased significantly. Seven days following all 3 surgical procedures, α3 transcript levels remained depressed, but PSD-93 transcript levels were still decreased only following axotomy or nerve crush. At 30 days post surgery, transcript levels for the nAChR subunits and PSD-93 had recovered. Acetylcholine-induced currents were significantly smaller in MPG neurons dissociated from 3-day explant cultured ganglia than from those recorded in neurons dissociated from acutely isolated ganglia; this observation provides direct evidence that a decrease in nAChR function was coincident with a decrease in nAChR subunit transcript levels. We conclude that a down regulation of nAChR subunit and PSD-93 expression following cavernous nerve injury, or even manipulation, could interrupt synaptic transmission within the MPG and thus contribute to the loss of neural control of urogenital organs following pelvic surgeries.