INCREASE OF B-50 GAP-43 IMMUNOREACTIVITY IN UNINJURED MUSCLE NERVES OF MDX MICE/

Lack of dystrophin in Mdx mice leads to muscle fibre degeneration foll owed by the formation of new myofibres. This degeneration-regeneration event occurs in clusters. It is accompanied by inflammation and remod elling of the intramuscular terminal nerve fibres. Since the growth-as sociated protein B-50/GAP-43 has been shown to be involved in axonal o utgrowth and synaptic remodelling following neuronal injury, we have i nvestigated the presence of B-50 in gastrocnemius and quadriceps muscl es of mdx mice. Using immunocytochemistry we demonstrate increased pre sence of B-50 in terminal nerve branches at motor endplates of mdx mic e, particularly in the clusters of de- and regenerating myofibres. In comparison, the control mice displayed no B-50 immunoreactivity in ner ve fibres contacting motor endplates. Our findings indicate that durin g axonal remodelling and collateral sprouting the B-50 level in the te rminal axon arbours is increased although there is no direct injury to the motoneurons. We suggest that the degenerating target and/or the i nflammatory reaction induces the increased B-50 level in the motoaxons . The increased B-50 may be important for sprouting of the nerve fibre s and re-establishment of synaptic contacts, and in addition, for matu ration and survival of the newly formed myofibres.