Severe micturition dysfunction can occur following spinal cord injury (SCI) due to abnormal contractions of the urethral sphincter during bladder contractions (bladder/sphincter dyssynergia). This causes urinary retention, bladder overdistension, and increases the workload of the bladder leading to hypertrophy of the bladder muscle. Bladder hypertrophy induced by urethral outlet ligation in rats is accompanied by enlargement of both the afferent and efferent neurons innervating the bladder. The primary aim of this study was to test whether SCI-induced bladder hypertrophy produces a similar enlargement of bladder afferent neurons in the dorsal root ganglia (DRG) or efferent neurons in the major pelvic ganglia (MPG). Following SCI in female Wistar rats, there was a four-fold increase in bladder weight. The mean cross-sectional area of bladder DRG cell profiles increased approx. 50% after SCI; however, the mean area of MPG cell profiles did not change significantly. Urinary diversion (disconnecting the ureters from the bladder) prevented both the bladder hypertrophy and the DRG cell hypertrophy after SCI, suggesting that bladder hypertrophy drives DRG cell enlargement. On the other hand, since the size of MPG cells did not change significantly after SCI, bladder hypertrophy does not mandate MPG cell enlargement. However, preliminary results indicate that the mean cross-sectional area of MPG cells did increase (2-3 times) in SCI rats when the neural input to the MPG was eliminated by transecting the pelvic and hypogastric nerves; this suggests that the lack of change in size of MPG cells after SCI may be due to an inhibitory influence from the spinal cord.