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Changes in expression and localization of glial cell line‐derived neurotrophic factor in skeletal muscle from rats at 3, 5 and 8 weeks of age
Author(s) -
Ousley Dominique D.,
Deering Scott J.,
Spitsbergen John M.
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.791.1
Subject(s) - glial cell line derived neurotrophic factor , neurotrophic factors , neuromuscular junction , gdnf family of ligands , biology , anatomy , endocrinology , skeletal muscle , medicine , neuroscience , microbiology and biotechnology , receptor
Glial cell line‐derived neurotrophic factor (GDNF) has been shown to play a role in motor neuron survival and plasticity. As GDNF plays a role in neural development we were interested in determining where and when GDNF was expressed in skeletal muscle during the final stages of neuromuscular junction development. We hypothesized that GDNF protein would be expressed at high levels at the end‐plate in 3 week old rats and that levels of expression would decline with increased age (5 and 8 weeks). Soleus , extensor digitorum longus and extensor hallucis longus muscles were removed and GDNF protein localization was examined using immunocytochemical methods. Muscles taken from 3 week old rats contained end‐plate regions at various stages of development, while muscles taken from older rats contained no immature end‐plates. The results showed little or no staining for GDNF protein at end‐plate regions in muscles from 3 week old rats. Muscles taken from older rats showed clear staining for GDNF protein at the end‐plate region. The results suggest that GDNF is not expressed at higher levels at developing end‐plates. These observations may suggest that GDNF plays a role at the neuromuscular junction beyond initial development, possibly being necessary for maintenance and growth of junctions as muscles continue to enlarge with animal growth. Supported by NIH Grant 1R15AG022908‐01A2, MSU‐KCMS, and Western Michigan University.