Department of Physiology, Kazan State Medical University, ul. Butlerova 49, R-420012 Kazan, Russia.
Muscle Nerve. 2011 Jun;43(6):872-7. doi: 10.1002/mus.22000. Epub 2011 Apr 12.
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.
Utilizing the combination of electrophysiology and myography, we investigated whether βAP also impairs the functioning of myocytes in frogs and mice.
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.
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.
阿尔茨海默病β-淀粉样肽（βAP）已知对体外和体内神经元具有广泛的毒性作用；然而，关于其对其他兴奋性组织（如骨骼肌）的影响的信息很少，除了脑细胞外，骨骼肌也被认为是βAP 的靶点。
我们利用电生理学和肌电图学的结合，研究了βAP 是否也会损害青蛙和小鼠的心肌细胞的功能。
尽管在 10(-6) 到 10(-8) M 的范围内应用βAP 会导致两种物种的肌肉纤维去极化，但它会通过降低终板电位幅度和增加阈电位来损害青蛙的收缩性，但不会损害小鼠的收缩性。
在存在βAP 的情况下，小鼠的收缩性不变是由于与两栖动物相比，哺乳动物的神经肌肉传递的安全系数更高。讨论了可能的临床意义。
