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.
journal_name
Neurosciencejournal_title
Neuroscienceauthors
Verzè L,Buffo A,Rossi F,Oestreicher AB,Gispen WH,Strata Pdoi
10.1016/s0306-4522(96)83017-xsubject
Has Abstractpub_date
1996-02-01 00:00:00pages
807-15issue
3eissn
0306-4522issn
1873-7544pii
S0306-4522(96)83017-Xjournal_volume
70pub_type
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