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Blocking Wnt Signaling in the Corticospinal Tract and Proprioceptive Sensory Axons /

Abstract

Spinal cord injury (SCI) can lead to physical dysfunction or paralysis. These features of SCI have been documented to relate to damage to the corticospinal tract of axons in the spinal cord. Wnt is a morphogen credited, amongst many other developmental tracts, with the anterior-posterior directional growth of the developing spinal cord. This gradient is mediated by Wnt's interaction with the Ryk receptor. It has been recently documented that in the mature spinal cord, following injury, Ryk-mediated Wnt repulsion of spared or sprouting axons restricts plasticity. This study sought out to block the Wnt signaling pathway via ligand -binding inhibitors via bone marrow stromal cell grafts and Ryk receptor silencing via monoclonal antibody infusion to increase corticospinal tract axon plasticity and to see if an increase in plasticity correlates with increased fine motor functional recovery. Most of the parameters used in the experiments involving the cell grafts were duplicated in an experiment utilizing the peripheral nervous system conditioning paradigm by injecting ethidium bromide into the sciatic nerve. We found discrepancies in behavioral studies correlated more strongly with lesion cavity size as opposed to axon plasticity after injury, opening avenues of research looking at the mechanisms behind the glial response to SCI and the potential role of Wnt signaling associated with the glial response to SCI

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