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二氢吡啶受体γ1亚基缺陷的小鼠肌纤维中Ca2+电流失活和Ca2+释放的改变

Altered inactivation of Ca2+ current and Ca2+ release in mouse muscle fibers deficient in the DHP receptor gamma1 subunit.

作者信息

Ursu Daniel, Schuhmeier Ralph Peter, Freichel Marc, Flockerzi Veit, Melzer Werner

机构信息

University of Ulm, Dept. of Applied Physiology, Albert-Einstein-Allee 11, D-89069 Ulm, Germany.

出版信息

J Gen Physiol. 2004 Nov;124(5):605-18. doi: 10.1085/jgp.200409168.

Abstract

Functional impacts of the skeletal muscle-specific Ca2+ channel subunit gamma1 have previously been studied using coexpression with the cardiac alpha1C polypeptide in nonmuscle cells and primary-cultured myotubes of gamma1-deficient mice. Data from single adult muscle fibers of gamma-/- mice are not yet available. In the present study, we performed voltage clamp experiments on enzymatically isolated mature muscle fibers of the m. interosseus obtained from gamma+/+ and gamma-/- mice. We measured L-type Ca2+ inward currents and intracellular Ca2+ transients during 100-ms step depolarizations from a holding potential of -80 mV. Ratiometric Ca2+ transients were analyzed with a removal model fit approach to calculate the flux of Ca2+ from the sarcoplasmic reticulum. Ca2+ current density, Ca2+ release flux, and the voltage dependence of activation of both Ca2+ current and Ca2+ release were not significantly different. By varying the holding potential and recording Ca2+ current and Ca2+ release flux induced by 100-ms test depolarizations to +20 mV, we studied quasi-steady-state properties of slow voltage-dependent inactivation. For the Ca2+ current, these experiments showed a right-shifted voltage dependence of inactivation. Importantly, we could demonstrate that a very similar shift occurred also in the inactivation curve of Ca2+ release. Voltages of half maximal inactivation were altered by 16 (current) and 14 mV (release), respectively. Muscle fiber bundles, activated by elevated potassium concentration (120 mM), developed about threefold larger contracture force in gamma-/- compared with gamma+/+. This difference was independent of the presence of extracellular Ca2+ and likely results from the lower sensitivity to voltage-dependent inactivation of Ca2+ release. These results demonstrate a specific alteration of voltage-dependent inactivation of both Ca2+ entry and Ca2+ release by the gamma1 subunit of the dihydropyridine receptor in mature muscle fibers of the mouse.

摘要

此前,通过在非肌肉细胞中与心脏α1C多肽共表达,以及在γ1缺陷小鼠的原代培养肌管中进行研究,探讨了骨骼肌特异性Ca2+通道亚基γ1的功能影响。目前尚无来自γ-/-小鼠单个成年肌纤维的数据。在本研究中,我们对从γ+/+和γ-/-小鼠获得的骨间肌酶解分离的成熟肌纤维进行了电压钳实验。我们在从-80 mV的 holding 电位进行100 ms的阶跃去极化过程中测量了L型Ca2+内向电流和细胞内Ca2+瞬变。采用去除模型拟合方法分析比率Ca2+瞬变,以计算Ca2+从肌浆网的通量。Ca2+电流密度、Ca2+释放通量以及Ca2+电流和Ca2+释放激活的电压依赖性均无显著差异。通过改变holding电位并记录由100 ms测试去极化至+20 mV诱导的Ca2+电流和Ca2+释放通量,我们研究了慢电压依赖性失活的准稳态特性。对于Ca2+电流,这些实验显示失活的电压依赖性右移。重要的是,我们能够证明Ca2+释放的失活曲线也发生了非常相似的偏移。半最大失活电压分别改变了16 mV(电流)和14 mV(释放)。由升高的钾浓度(120 mM)激活的肌纤维束,与γ+/+相比,γ-/-中的挛缩力大约大三倍。这种差异与细胞外Ca2+的存在无关,可能是由于对Ca2+释放的电压依赖性失活的敏感性较低所致。这些结果表明,小鼠成熟肌纤维中二氢吡啶受体的γ1亚基对Ca2+内流和Ca2+释放的电压依赖性失活有特定改变。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bdbc/2234002/ce204d6a217e/200409168f2.jpg

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