Double immunolocalization of B-50 and A4 protein in Alzheimer's disease: A.B. Oestreicher, W.H. Gispen and J.M. Rozemuller ∗. Rudolf Magnus Institute, Medical Faculty, University of Utrecht and ∗Dept. of Neuropathology, Medical Faculty, Free University, Amsterdam, The Netherlands

Abstract

Lack of dystrophin in mdx mice leads to muscle fibre degeneration followed by the formation of new myofibres. This degeneration—regeneration event occurs in clusters. It is accompanied by inflammation and remodelling of the intramuscular terminal nerve fibres. Since the growth-associated protein B-50/GAP-43 has been shown to be involved in axonal outgrowth and synaptic remodelling following neuronal injury, we have investigated the presence of B-50 in gastrocnemius and quadriceps muscles of mdx mice. Using immunocytochemistry we demonstrate increased presence of B-50 in terminal nerve branches at motor endplates of mdx mice, particularly in the clusters of de- and regenerating myofibres. In comparison, the control mice displayed no B-50 immunoreactivity in nerve fibres contacting motor endplates. Our findings indicate that during axonal remodelling and collateral sprouting the B-50 level in the terminal axon arbours is increased although there is no direct injury to the motoneurons.We suggest that the degenerating target and/or the inflammatory reaction induces the increased B-50 level in the motoaxons. The increased B-50 may be important for sprouting of the nerve fibres and re-establishment of synaptic contacts, and in addition, for maturation and survival of the newly formed myofibres.