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Synaptic vesicle morphology and recycling are altered in myenteric neurons of mice lacking dystrophin (mdx mice)
Author(s) -
Vannucchi Maria Giuliana,
Corsani Letizia,
FaussonePellegrini MariaSimonetta
Publication year - 2003
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.10305
Subject(s) - myenteric plexus , dystrophin , synaptic vesicle , gene isoform , duchenne muscular dystrophy , biology , muscular dystrophy , endoplasmic reticulum , motility , mdx mouse , microbiology and biotechnology , medicine , endocrinology , vesicle , immunohistochemistry , pathology , immunology , biochemistry , membrane , gene , genetics
Several dystrophin isoforms are known. The full‐length isoform is present in striated and smooth muscles and neurons and its lack causes Duchenne Muscular Dystrophy, a progressive myopathy accompanied by mild cognitive deficits and gastrointestinal dismotility. An ultrastructural study was undertaken in the colon of mice lacking full‐length dystrophin and maintaining shorter isoforms (mdx mice) to ascertain whether myenteric neurons have an altered morphology. Results showed a significant increase in the size of synaptic vesicle and in the number of recycling vesicles. An enlargement of endoplasmic reticulum cisternae in a subpopulation of neurons was also seen. Immunohistochemistry confirmed that the shorter isoforms were expressed in mdx mice myenteric neurons. These findings indicate the presence of a neuropathy at the myenteric plexus which might justify the defective neuronal control of gastrointestinal motility reported for these animals and which might be correlated with full‐length dystrophin loss, since the shorter isoforms are present. J. Cell. Physiol. 197: 232–242, 2003. © 2003 Wiley‐Liss, Inc.