Dysfunction of the sacral autonomic systems controlling micturition, defecation and copulation is an area of particular concern in the management of patients with spinal injuries or urinary incontinence. The anatomical basis involved in normal pelvic visceral function and the changes in circuitry during postnatal development and following spinal injury have not been adequately explored. The final path of the pelvic autonomic circuitry and the focus of this proposal is the sacral parasympathetic preganglionic (SPP) neuron. The first hypothesis of this proposal is that primary afferent, descending and propriospinal input, each with specific molecular markers, directly synapse on sacral parasympathetic preganglionic neurons. The second hypothesis is that alterations in this circuitry occur during postnatal development and following spinal transection, so that these can be quantified by light and electron microscopic immunohistochemistry. Specifically, the distribution, location, and density of immunostained primary afferent, descending, and propriospinal terminals that synapse on intracellularly labeled sacral parasympathetic preganglionic neurons will be determined. These data will be compared with normal neonatal and adult rats as well as acute and chronic spinal transected adult rats. An understanding of the normal and post-injury changes in the organization of peptidergic or aminergic terminals may lead to new pharmacological approaches to promote the recovery of visceral function in patients with spinal cord injuries or with urinary incontinence.
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