Although gonadal steroids are important determinants of the development and activity of various neuronal circuits in the brain and spinal cord, their function has been relatively poorly studied in the peripheral nervous system. In the present work, the effects of pre- and postpubertal castration were examined on the morphology of autonomic neurons that supply pelvic visceral organs in male rats. These neurons were identified by peripheral injection of fluorescent retrograde tracers and, in the major pelvic ganglion, were further classified as sympathetic or parasympathetic by means of immunostaining for tyrosine hydroxylase. Sizes of ganglion cell somata were indicated by areas of nucleated profiles in cryosections. The results show that, irrespective of whether castration was carried out at two or seven weeks-of-age, noradrenergic pelvic neurons that supply the vas deferens, prostate gland, urinary bladder or colon achieved only ~60% of the size of those in unoperated controls. In contrast, cholinergic pelvic neurons were unaffected by castration unless they supplied reproductive targets. Pre- and paravertebral sympathetic neurons that supplied the pelvic viscera were only slightly smaller following castration or were unchanged, depending on their target. All effects of castration were prevented by testosterone replacement following surgery. Androgen receptor-immunoreactivity was particularly prevalent in the nuclei of some pelvic ganglion neurons. The studies suggest that circulating androgens are essential for the maturation and maintenance of the structure of select groups of autonomic neurons that supply the viscera. The presence of androgen receptor immunoreactivity in many of these neurons indicates that direct neuronal effects of androgens are possible. However this does not exclude other less direct mechanisms of steroid action on neurons, such as by an effect on target organs, neurotrophic factor release or peripheral vascular supply. These studies point to the androgenic steroids as potentially important determinants of autonomic reflex function.
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