Morphological Plasticity in Efferent Pathways to of the Rat Following Urethral Obstruction the Urinary Bladder

Partial urethral ligation in female Wistar rats produces changes in the neural control of the lower urinary tract including bladder hyperactivity and facilitation of a spinal micturition reflex pathway. To gain insight into the mechanisms underlying these changes, axonal tracing studies were conducted to examine the postganglionic efferent limb of the micturition reflex pathway which originates in the major pelvic ganglion (MPG). Forty microliters of the tracer FluoroGold (4%) were injected into the right side of the bladder in urethral-obstructed (n = 10) and control (n = 4) rats 6 weeks after urethral ligation or sham surgery. As a control Fast blue (40 ~1, 5%) was injected into the colon to label neurons in the MPG innervating the intestine. Obstructed rats exhibited a 6-fold increase (p < 0.001) in bladder weight (0.646 gm) compared to controls (0.146 gm). A significant increase (p < 0.001) in the size of labeled bladder postganglionic neurons in the MPG was noted in obstructed rats (576.4 pm2, n = 4) as compared to controls (299.6 pm2). However, labeled, colon postganglionic neurons in the MPG in obstructed (312.9 wm2) rats were not enlarged compared to controls (359.4 Fm2). Neuronal hypertrophy was not associated with a change in the number of labeled MPG neurons in control and obstructed groups. Capsaicin (150 mg/kg S.C. in divided doses) (n = 3) or unilateral pelvic nerve transection prior to urethral ligation (n = 3) did not prevent the enlargement of the bladder or of the postganglionic neurons, suggesting that neither capsaicin-sensitive afferents nor parasympathetic preganglionic efferent activity was essential for neuronal hypertrophy. Therefore, it is speculated that the neuronal changes induced by urethral obstruction are mediated by a peripheral mechanism such as an increased production of trophic factors in the bladder.