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Early endplate remodeling and skeletal muscle signaling events following rat hindlimb suspension
Author(s) -
Chibalin Alexander V.,
Benziane Boubacar,
Zakyrjanova Guzalija F.,
Kravtsova Violetta V.,
Krivoi Igor I.
Publication year - 2018
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.26594
Subject(s) - ampk , autophagy , phosphorylation , soleus muscle , skeletal muscle , hindlimb , acetylcholine receptor , endocrinology , protein kinase a , medicine , amp activated protein kinase , motor endplate , biology , microbiology and biotechnology , chemistry , neuromuscular junction , receptor , biochemistry , neuroscience , apoptosis
Motor endplates naturally undergo continual morphological changes that are altered in response to changes in neuromuscular activity. This study examines the consequences of acute (6–12 hr) disuse following hindlimb suspension on rat soleus muscle endplate structural stability. We identify early changes in several key signaling events including markers of protein kinase activation, AMPK phosphorylation and autophagy markers which may play a role in endplate remodeling. Acute disuse does not change endplate fragmentation, however, it decreases both the individual fragments and the total endplate area. This decrease was accompanied by an increase in the mean fluorescence intensity from the nicotinic acetylcholine receptors which compensate the endplate area loss. Muscle disuse decreased phosphorylation of AMPK and its substrate ACC, and stimulated mTOR controlled protein synthesis pathway and stimulated autophagy. Our findings provide evidence that changes in endplate stability are accompanied by reduced AMPK phosphorylation and an increase in autophagy markers, and these changes are evident within hours of onset of skeletal muscle disuse.