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PURPOSE: Robust muscle atrophy and fibrosis are cited as the prime causes for the permanence of motor deficits following surgical intervention for a denervation injury. Following a peripheral nerve transection, regenerating axons traverse long distances to reinnervate their target organs. However, due to the slow rate of axonal regrowth and a large segmental defect, muscle atrophy and destabilization of the neuromuscular junction (NMJ) usually proceeds before reinnervation occurs. Agrin is characterized as an essential component of NMJ formation and synaptogenesis. Here, we utilize an in vivo agrin deficient mouse nerve denervation model to both characterize the morphology of agrin deficient endplates as well as the response of the NMJ to local delivery of agrin following a denervation event. We found the endplates of agrin-deficient mice in a more degraded states than the endplates of wildtype mice following denervation. We also found that local delivery of agrin following denervation serves to transiently improve motor endplate morphology. We thus demonstrate the efficacy of using a biomolecular therapeutic approach to maintain and preserve the denervated NMJ.

Abstract 136: Denervation Induced Degradation of Motor Endplates can be Delayed Using Local Supplementation of Agrin at the Time of Injury.