Descending spinal projections from the rostral gigantocellular reticular nuclei complex

Electrophysiological and physiological studies have suggested that the ventral medullary gigantocellular reticular nuclei (composed of the gigantocellular ventralis and pars alpha nuclei as well as the adjacent lateral paragigantocellular nucleus; abbreviated Gi-LPGi complex) provide descending control of pelvic floor organs (Mackel [1979] J. Physiol. (Lond.) 294:105-122; Hubscher and Johnson [1996] J. Neurophysiol. 76:2474-2482; Hubscher and Johnson [1999] J. Neurophysiol. 82:1381-1389; Johnson and Hubscher [1998] Neuroreport 9:341-345). Specifically, this complex of paramedian reticular nuclei has been implicated in the inhibition of sexual reflexes. In the present study, an anterograde fluorescent tracer was used to investigate direct descending projections from the Gi-LPGi complex to retrogradely labeled pudendal motoneurons (MN) in the male rat. Our results demonstrated that, although a high density of arborizations from Gi-LPGi fibers appears to be in close apposition to pudendal MNs, this relationship also applies to other MNs throughout the entire spinal cord. The Gi-LPGi also projects to spinal autonomic regions, i.e., both the intermediolateral cell column and the sacral parasympathetic nucleus, as well as to regions of the intermediate gray, which contain interneurons involved in the organization of pelvic floor reflexes. Lastly, throughout the length of the spinal cord, numerous neurons located primarily in laminae VII-X, were retrogradely labeled with Fluoro-Ruby after injections into the Gi-LPGi. The diffuse descending projections and arborizations of this pathway throughout the spinal cord suggest that this brainstem area is involved in the direct, descending control of a variety of spinal activities. These results are in contrast with our observations of the discrete projections of the caudal nucleus raphe obscurus, which target the autonomic and somatic MNs involved specifically in sexual and eliminative functions (Hermann et al. [1998] J. Comp. Neurol. 397:458-474).