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Fiber Type Composition of the Sternomastoid and Diaphragm Muscles of Dystrophin‐Deficient mdx Mice
Author(s) -
Guido Anderson Neri,
Campos Gerson Eduardo Rocha,
Neto Humberto Santo,
Marques Maria Julia,
Minatel Elaine
Publication year - 2010
Publication title -
the anatomical record: advances in integrative anatomy and evolutionary biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.678
H-Index - 62
eISSN - 1932-8494
pISSN - 1932-8486
DOI - 10.1002/ar.21224
Subject(s) - mdx mouse , dystrophin , neuromuscular junction , diaphragm (acoustics) , duchenne muscular dystrophy , population , sprouting , anatomy , biology , neuromuscular disease , skeletal muscle , fiber , chemistry , medicine , neuroscience , disease , genetics , physics , botany , environmental health , acoustics , loudspeaker , organic chemistry
The muscle fiber phenotype is mainly determined by motoneuron innervation and changes in neuromuscular interaction alter the muscle fiber type. In dystrophin‐deficient mdx mice, changes in the molecular assembly of the neuromuscular junction and in nerve terminal sprouting occur in the sternomastoid (STN) muscle during early stages of the disease. In this study, we were interested to see whether early changes in neuromuscular assembly are correlated with alterations in fiber type in dystrophic STN at 2 months of age. A predominance of hybrid fast myofibers (about 52% type IIDB) was observed in control (C57Bl/10) STN. In mdx muscle, the lack of dystrophin did not change this profile (about 54% hybrid type IIDB). Pure fast type IID fibers predominated in normal and dystrophic diaphragm (DIA; about 39% in control and 30% in mdx muscle) and a population of slow Type I fibers was also present (about 10% in control and 13% in mdx muscle). In conclusion, early changes in neuromuscular assembly do not affect the fiber type composition of dystrophic STN. In contrast to the pure fast fibers of the more affected DIA, the hybrid phenotype of the STN may permit dynamic adaptations during progression of the disease. Anat Rec 293:1722–1728, 2010. © 2010 Wiley‐Liss, Inc.