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Extraneuronal toxicity of Alzheimer's β‐amyloid peptide: Comparative study on vertebrate skeletal muscles
Author(s) -
Mukhamedyarov Marat A.,
Teplov Alexander Y.,
Grishin Sergey N.,
Leushina Alina V.,
Zefirov Andrey L.,
Palotás András
Publication year - 2011
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.22000
Subject(s) - depolarization , contractility , neuromuscular transmission , biology , skeletal muscle , electrical impedance myography , in vivo , electrophysiology , amyloid (mycology) , neuroscience , myocyte , toxicity , medicine , endocrinology , anatomy , botany , microbiology and biotechnology , vasodilation
. Alzheimer's β‐amyloid peptide (βAP) is known to possess a wide range of toxic effects on neurons in vitro and in vivo; however, there is little information available regarding its impact on other excitable tissues such as skeletal muscles, which, apart from brain cells, are thought to also be targets of βAP. Methods. Utilizing the combination of electrophysiology and myography, we investigated whether βAP also impairs the functioning of myocytes in frogs and mice. Results. Although application of βAP in the range of 10 −6 to 10 −8 M induced depolarization of muscle fibers in both species, it impaired contractility in frogs but not in mice, by reducing endplate potential amplitude and increasing the threshold potential. Conclusions. Unchanged contractility in the mouse in the presence of βAP is due to a higher safety factor of neuromuscular transmission in mammals compared with amphibians. Possible clinical implications are discussed. Muscle Nerve, 2011.