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哺乳动物骨骼肌纤维中长度依赖性的钙离子激活

Length-dependent Ca2+ activation in skeletal muscle fibers from mammalians.

作者信息

Rassier Dilson E, Minozzo Fábio C

机构信息

Departments of Kinesiology and Physical Education, McGill University, Montreal, Canada; Department of Physics, McGill University, Montreal Canada; Department of Physiology, McGill University, Montreal, Canada; and

Departments of Kinesiology and Physical Education, McGill University, Montreal, Canada; McGill Health Centre Research Institute, Montreal, Canada.

出版信息

Am J Physiol Cell Physiol. 2016 Aug 1;311(2):C201-11. doi: 10.1152/ajpcell.00046.2016. Epub 2016 May 25.

Abstract

We tested the hypotheses that 1) a decrease in activation of skeletal muscles at short sarcomere lengths (SLs) is caused by an inhibition of Ca(2+) release from the sarcoplasmic reticulum (SR), and 2) the decrease in Ca(2+) would be caused by an inhibition of action potential conduction from the periphery to the core of the fibers. Intact, single fibers dissected from the flexor digitorum brevis from mice were activated at different SLs, and intracellular Ca(2+) was imaged with confocal microscopy. Force decreased at SLs shorter than 2.1 μm, while Ca(2+) concentration decreased at SLs below 1.9 μm. The concentration of Ca(2+) at short SL was lower at the core than at the peripheries of the fiber. When the external concentration of Na(+) was decreased in the experimental media, impairing action potential conduction, Ca(2+) gradients were observed in all SLs. When caffeine was used in the experimental media, the gradients of Ca(2+) were abolished. We concluded that there is an inhibition of Ca(2+) release from the sarcoplasmic reticulum (SR) at short SLs, which results from a decreased conduction of action potential from the periphery to the core of the fibers.

摘要

我们检验了以下假设

1)在短肌节长度(SLs)下骨骼肌激活的降低是由肌浆网(SR)中Ca(2+)释放的抑制所导致的;2)Ca(2+)的降低是由动作电位从纤维外周向核心传导的抑制所引起的。从小鼠趾短屈肌分离出的完整单根纤维在不同的SLs下被激活,并用共聚焦显微镜对细胞内Ca(2+)进行成像。在短于2.1μm的SLs下,力降低,而在低于1.9μm的SLs下,Ca(2+)浓度降低。在短SLs下,纤维核心处的Ca(2+)浓度低于外周。当实验介质中Na(+)的外部浓度降低,损害动作电位传导时,在所有SLs下均观察到Ca(2+)梯度。当在实验介质中使用咖啡因时,Ca(2+)梯度消失。我们得出结论,在短SLs下存在肌浆网(SR)中Ca(2+)释放的抑制,这是由动作电位从纤维外周向核心传导的降低所导致的。

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