Extraneuronal toxicity of Alzheimer's β-amyloid peptide: Comparative study on vertebrate skeletal muscles

Introduction. 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 though...

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Bibliographic Details
Published in:Muscle & nerve 2011-06, Vol.43 (6), p.872-877
Main Authors: Mukhamedyarov, Marat A., Teplov, Alexander Y., Grishin, Sergey N., Leushina, Alina V., Zefirov, Andrey L., Palotás, András
Format: Article
Language:English
Subjects:
Alzheimer disease
Amyloid beta-Peptides - physiology
Amyloid beta-Peptides - toxicity
Animals
Brain - metabolism
Brain - pathology
Brain - physiopathology
contractility
depolarization
Diaphragm - metabolism
Diaphragm - physiopathology
Electromyography - methods
Mice
Muscle Fibers, Skeletal - metabolism
Muscle Fibers, Skeletal - pathology
Muscle Fibers, Skeletal - physiology
Muscle, Skeletal - metabolism
Muscle, Skeletal - physiopathology
Neurons - metabolism
Neurons - pathology
Neurons - physiology
Peptide Fragments - physiology
Peptide Fragments - toxicity
Rana ridibunda
skeletal muscle
Species Specificity
β-amyloid peptide
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Summary:Introduction. 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.
ISSN:0148-639X
1097-4598
DOI:10.1002/mus.22000