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贻贝捕捉肌的捕捉状态在激活过程中确立:使用肌球蛋白抑制剂原钒酸盐和布列他汀对紫贻贝前足丝牵缩肌的去膜纤维制剂进行的实验。

The catch state of mollusc catch muscle is established during activation: experiments on skinned fibre preparations of the anterior byssus retractor muscle of Mytilus edulis L. using the myosin inhibitors orthovanadate and blebbistatin.

作者信息

Andruchov Oleg, Andruchova Olena, Galler Stefan

机构信息

Department of Cell Biology, University of Salzburg, Hellbrunnerstrasse 34, A-5020 Salzburg, Austria.

出版信息

J Exp Biol. 2006 Nov;209(Pt 21):4319-28. doi: 10.1242/jeb.02501.

Abstract

Catch is a holding state of muscle where tension is maintained passively for long time periods in the absence of stimulation. The catch state becomes obvious after termination of activation; however, it is possible that catch linkages are already established during activation. To investigate this, skinned fibre bundles of the anterior byssus retractor muscle of Mytilus edulis were maximally activated with Ca(2+) and subsequently exposed to 10 mmol l(-1) orthovanadate (V(i)) or 5 mumol l(-1) blebbistatin to inhibit the force-generating myosin head cross-bridges. Repetitive stretches of about 0.1% fibre bundle length were applied to measure stiffness. Inhibitor application depressed force substantially but never resulted in a full relaxation. The remaining force was further decreased by moderate alkalization (change of pH from 6.7 to 7.4) or by cAMP. Furthermore, the stiffness/force ratio was higher during exposure to V(i) or blebbistatin than during partial Ca(2+) activation producing the same submaximal force. The increased stiffness/force ratio was abolished by moderate alkalization or cAMP. Finally, the stretch-induced delayed force increase (stretch activation) disappeared, and the force recovery following a quick release of the fibre length, was substantially reduced when the force was depressed by V(i) or blebbistatin. All these findings suggest that catch linkages are already established during maximal Ca(2+) activation. They seem to exhibit ratchet properties because they allow shortening and resist stretches. In isometric experiments a force decrease is needed to stress the catch linkages in the high resistance direction so that they contribute to force.

摘要

强直收缩是肌肉的一种保持状态,即在无刺激情况下张力被被动维持很长时间。激活终止后,强直收缩状态变得明显;然而,强直收缩连接可能在激活过程中就已建立。为了对此进行研究,用Ca(2+)使紫贻贝前足丝牵缩肌的脱膜纤维束最大程度激活,随后将其暴露于10 mmol l(-1)的原钒酸盐(V(i))或5 mumol l(-1)的肌球蛋白抑制剂中,以抑制产生力的肌球蛋白头部横桥。施加约0.1%纤维束长度的重复拉伸来测量刚度。施加抑制剂使力大幅降低,但从未导致完全松弛。通过适度碱化(pH从6.7变为7.4)或cAMP可进一步降低剩余的力。此外,在暴露于V(i)或肌球蛋白抑制剂期间,刚度/力比高于产生相同次最大力的部分Ca(2+)激活期间。适度碱化或cAMP可消除增加的刚度/力比。最后,当力被V(i)或肌球蛋白抑制剂降低时,拉伸诱导的延迟力增加(拉伸激活)消失,并且纤维长度快速释放后的力恢复也大幅降低。所有这些发现表明,强直收缩连接在最大Ca(2+)激活期间就已建立。它们似乎具有棘轮特性,因为它们允许缩短并抵抗拉伸。在等长实验中,需要力降低以在高阻力方向上拉紧强直收缩连接,从而使其产生力。

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