The aim of our study was to provide quantitative data on pudendal motor neuron cell bodies and axons in the female rat. To confirm earlier studies, fluorescent retrograde tracers were used to label the motor neurons for correlation with myelinated axon counts along the length of the motor pudendal nerve. The external urethral sphincter of female rats was injected with diamidino yellow and the external anal sphincter with fast blue. The L 6 spinal cord revealed labeled motor neurons. Those in the dorsolateral column (60.8 Ϯ 10.6) had nuclei labeled yellow from the external urethral sphincter and those in the dorsomedial column (31.7 Ϯ 8.5) had cytoplasm labeled blue from the external anal sphincter. Double labeling was not present, suggesting that pudendal motor neurons in each column innervate separate sphincters. The motor pudendal nerve in the ischiorectal fossa was also characterized by light microscopy. The mean myelinated axon count (151.4 Ϯ 17.0) was highly correlated (r ϭ 0.995) in the proximal fascicles and the sum of distal fascicles. This indicated that myelinated axons do not branch at the point where the main motor pudendal nerve branches into separate fascicles. Axon counts between sides were not as well correlated (r ϭ 0.883). The ratio of motor neurons to myelinated axons is 56%, suggesting that some myelinated axons either innervate other muscles or are sensory. This reproducible characterization of the normal pudendal nerve anatomy provides an excellent basis for experimental studies associated with pudendal nerve denervation as a model for neurogenic incontinence.

with a sham capsule. After 2 weeks the pudendal nerves and urethral tissues were prepared for light and electron microscopy. The number of axons, myelin figures and endoneurial nuclei in the pudendal nerve segment distal to the lesion were counted. Nerve fascicles near the EUS were also counted and categorized as normal or showing signs of degeneration and/or regeneration. The location of each nerve fascicle was specified as either ventral or dorsal. RESULTSAs there were no significant differences between the two control groups they were combined to form a single control group. In the distal pudendal nerve there were significantly fewer myelinated axons and large myelinated axons in the NC + E and NC + S groups than in the control group. There were three times as many large unmyelinated axons in the NC + E group than in either the NC + S or control groups ( P < 0.05). There were only half as many nerve fascicles near the ventral side of the EUS in the NC + S group than in both the control and NC + E groups ( P < 0.05). CONCLUSIONOestrogen appears to affect large unmyelinated axons in both the injured pudendal nerve and at the denervated EUS target. After pudendal nerve crush, nerve fascicles with evidence of degeneration or regeneration near the EUS appear to be spared with oestrogen treatment, particularly in the ventral region. These observations may reflect the early stages of a neuroregenerative effect of oestrogen. Additional studies are needed to confirm these results at later periods and with functional methods. KEYWORDSurinary incontinence, external urethral sphincter, ultrastructure, nerve injury, oestrogen, pudendal nerve OBJECTIVETo determine the early effects of oestrogen on the ultrastructure of the pudendal nerve and distal nerve fascicles near the external urethra sphincter (EUS) after a pudendal nerve crush injury. The pudendal nerve is one of the pelvic floor tissues injured during vaginal delivery, possibly contributing to the development of stress urinary incontinence (SUI) in women, the symptoms of which often do not appear until menopause, implicating hormonal factors.