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Rachel M. Behrend
Clinical studies have demonstrated that it is possible to retrieve lost motor function in patients with spinal cord damage by using sensory stimulation. Recent research conducted on the neonatal mouse spinal cord has shown that stimulation of sensory fibers such as the sacrocaudal afferents (SCAs) results in the activation of spinal neuronal networks known as central pattern generators (CPGs), thereby producing rhythmic locomotor outputs. While intact long ascending fibers are essential for information processing in the brain, locomotion can still be produced by recruitment of spinal neurons in cases of spinal cord injury where white matter tracts are damaged. It is established that there is no direct connectivity between SCAs and hindlimb CPGs. However, it is suggested that sacral relay neurons bridge their connectivity by recruiting either other groups of propriospinal neurons, or by projecting directly to rostral areas of the cord or to supra spinal areas through various white matter funiculi. Since past work has shown that lesions to the ventral funiculus (VF) can more severely hinder CPG activation than can lesions to other white matter funiculi, we only examined sacral neurons projecting through the ventral funiculus.
While these sacral relay neurons can now be anatomically identified, much remains unknown about their role in targeting CPGs. Here, we aimed to further elucidate the architecture of these sacral relay neurons by using anatomical and immunohistochemical methods to examine their morphology and connectivity. Specifically, we examined the synaptic inputs they receive, their size, and their projection patterns in the spinal cord and brain. Previous work showed that stimulation of pain fibers could activate CPGs, and that agonists to certain nociceptive receptors could block CPG activation. Other studies show that VGluT2 can be found on nociceptive fibers. Also, at neonatal age VGluT1 is exclusively expressed by primary afferents. For these reasons, we looked to see if afferent fibers expressing VGluT1 and VGluT2 directly contact the neurons. IB4, NK1 and CGRP will also be studied (work in progress).
Last Modified December 23, 2013