Shalton P M, Wareham A C
Muscle Nerve. 1980 Mar-Apr;3(2):120-7. doi: 10.1002/mus.880030204.
Neuromuscular junctions of slow- and fast-twitch skeletal muscles from dystrophic (dy2J/dy2J) and control mice of the C57BL/6J strain were used to investigate the effect of muscular dystrophy on nerve-terminal regulation of their intracellular concentration of free calcium ions. The frequency of spontaneous miniature endplate potentials (MEPPs) was taken as an indicator of the intraterminal free calcium ion concentration. Dicoumarol, 2,4-dinitrophenol, ruthenium red, and the calcium ionophore A-23187 all potentiated the MEPP frequency in dystrophic muscles at concentrations which had negligible effects on normal muscles. Dystrophic muscle preparations were also more sensitive to an increased extracellular calcium concentration. Usually, these manipulations had more effect on the nerve terminals of dystrophic slow muscle than on those of dystrophic fast muscle. We conclude that muscular dystrophy alters the nerve terminal's ability to regulate the concentration of intracellular free calcium ions.
来自营养不良(dy2J/dy2J)的C57BL/6J品系小鼠和对照小鼠的慢肌和快肌骨骼肌神经肌肉接头被用于研究肌肉营养不良对其细胞内游离钙离子浓度的神经末梢调节的影响。自发微小终板电位(MEPPs)的频率被用作终板内游离钙离子浓度的指标。双香豆素、2,4-二硝基苯酚、钌红和钙离子载体A-23187在对正常肌肉影响可忽略不计的浓度下,均增强了营养不良肌肉中的MEPP频率。营养不良的肌肉制剂对细胞外钙浓度升高也更敏感。通常,这些操作对营养不良慢肌的神经末梢的影响比对营养不良快肌的神经末梢的影响更大。我们得出结论,肌肉营养不良会改变神经末梢调节细胞内游离钙离子浓度的能力。