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沉默钙通道在甲壳类动物骨骼肌纤维中的管状定位。

Tubular localization of silent calcium channels in crustacean skeletal muscle fibers.

作者信息

Monterrubio J, Ortiz G, Orkand P M, Zuazaga C

机构信息

Institute of Neurobiology, Department of Physiology, University of Puerto Rico, San Juan 00901, USA.

出版信息

J Muscle Res Cell Motil. 2002;23(2):167-74. doi: 10.1023/a:1020225231520.

Abstract

Ca2+-induced Ca2+ release (CICR) in the superficial abdominal flexor muscle of the crustacean Atya lanipes appears to be mediated by a local control mechanism similar to that of vertebrate cardiac muscle, but with an unusually high gain. Thus, Ca2+ influx increases sufficiently the local concentration of Ca2+ in the immediate vicinity of the sarcoplasmic reticulum Ca2+ release channels to trigger the highly amplified release of Ca2+ required for contraction, but is too low to generate a macroscopic inward current (i.e., the Ca2+ channels are silent). To determine the localization of the silent Ca2+ Channels, the mechanical, electrophysiological and ultrastructural properties of the muscle were examined before and after formamide treatment, a procedure that produces the disruption of transverse tubules of striated muscle. We found that tubular disruption decreased tension generation by about 90%; reduced inward current (measured as Vmax, the maximum rate of rise of Sr2+ action potentials) by about 80%; and decreased membrane capacitance by about 77%. The results suggest that ca. 80% of the silent Ca2+ channels are located in the tubular system. Thus, these studies provide further evidence to support the local control mechanism of CICR in crustacean skeletal muscle.

摘要

在甲壳动物阿蒂亚拉尼佩什的腹部浅层屈肌中,钙诱导的钙释放(CICR)似乎是由一种类似于脊椎动物心肌的局部控制机制介导的,但具有异常高的增益。因此,钙内流足以增加肌浆网钙释放通道紧邻区域的局部钙浓度,从而触发收缩所需的高度放大的钙释放,但钙内流过低,无法产生宏观内向电流(即钙通道处于静息状态)。为了确定静息钙通道的定位,在甲酰胺处理前后对肌肉的机械、电生理和超微结构特性进行了检查,甲酰胺处理会导致横纹肌横管的破坏。我们发现,管腔破坏使张力产生降低了约90%;内向电流(以Vmax衡量,即Sr2+动作电位的最大上升速率)降低了约80%;膜电容降低了约77%。结果表明,约80%的静息钙通道位于管状系统中。因此,这些研究提供了进一步的证据来支持甲壳动物骨骼肌中CICR的局部控制机制。

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