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Nerve terminal and shwann cell response after nerve injury in the absence of nitric oxide.


Dystrophic muscles show alterations in the dystrophin-glycoprotein complex and a lack of neuronal nitric oxide (NO) synthase, associated with structural changes in neuromuscular junction. In this study, we examined the nerve terminal and Schwann cell responses after a crush lesion in NO-deficient mice. Seven days after nerve crush, 24% of the control junctions (n=200) showed ultraterminal sprouts. In the absence of NO, this frequency was 28.5% (n=217; p>0.05 compared to the controls; X2 test). Schwann cell response did not change in the absence of NO, after 7 days of nerve lesion. Fourteen days after nerve lesion, nerve terminals sprouted and Schwann cells showed an extensive network of processes away from the synaptic site. In the absence of NO, there was a dramatic decrease in nerve terminal sprouting and Schwann cells processes failed to extend away from the endplate. These results show that NO is involved in nerve terminal and Schwann cell response to nerve injury. They also suggest that presynaptic molecular signaling may be impaired in dystrophic muscles, and this could influence the innervation and survival of newly formed myofibers generated by cell-mediated therapies. (AU)

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