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紫贻贝前足丝牵缩肌收缩机制的激活。

Activation of the contractile mechanism in the anterior byssal retractor muscle of Mytilus edulis.

作者信息

Sugi H, Yamaguchi T

出版信息

J Physiol. 1976 Jun;257(3):531-47. doi: 10.1113/jphysiol.1976.sp011383.

Abstract
  1. The electrical and mechanical responses of the anterior byssal retractor muscle (ABRM) of Mytilus edulis to acetylcholine (ACh), high [K]O or the removal of external Ca were examined under a variety of conditions. 2. ACh (10(-6)--10(-3)M) produced contracture tensions larger than those produced by high [K]O (30-300 mM) for a given amount of depolarization. In Ca-free solution, the rate of decline of ACh-contractures was much smaller than that of K contractures, though both ACh- and K-contractures eventually disappeared. 3. 5-HT (10(-4)M) of procaine (1 mM) markedly reduced the height of ACh-contractures, but had little or no effect on K-contractures. The height of K contractures was markedly decreased by Mn ions (20 mM) or low pH (4-5), while ACh-contractures remained unaffected. 4. Partial replacement of [Na]o by choline (30-100 mM) reduced both ACh-induced depolarization and contracture tension, whereas K-contractures remained unchanged even after total replacement of [Na]o by choline. 5. ACh could produce little or no tension when applied during the relaxation phase of K-contractures, while high [K]o produced the maximal contracture tension when applied during the relaxation phase of ACh-contractures. 6. Following the removal of external Ca from solutions containing less than 10 mM-Mg, the ABRM showed a marked tension development associated with repetitive electrical activity superimposed on a gradual decline of membrane potential. 7. These results suggest that ACh-contractures are mainly due to the release of intracellularly stored Ca, while K-contractures are mainly associated with the inward movement of external Ca.
摘要
  1. 在多种条件下,研究了紫贻贝前足丝牵缩肌(ABRM)对乙酰胆碱(ACh)、高[K]O或去除细胞外Ca的电反应和机械反应。2. 对于给定的去极化量,ACh(10^(-6) - 10^(-3)M)产生的挛缩张力大于高[K]O(30 - 300 mM)产生的张力。在无Ca溶液中,ACh挛缩的下降速率远小于K挛缩的下降速率,尽管ACh和K挛缩最终都会消失。3. 5 - HT(10^(-4)M)或普鲁卡因(1 mM)显著降低了ACh挛缩的高度,但对K挛缩几乎没有影响。Mn离子(20 mM)或低pH(4 - 5)显著降低了K挛缩的高度,而ACh挛缩则不受影响。4. 用胆碱(30 - 100 mM)部分替代[Na]o降低了ACh诱导的去极化和挛缩张力,而即使完全用胆碱替代[Na]o,K挛缩仍保持不变。5. 在K挛缩的松弛期施加ACh时几乎不产生或不产生张力,而在ACh挛缩的松弛期施加高[K]O时产生最大挛缩张力。6. 从含有低于10 mM - Mg的溶液中去除细胞外Ca后,ABRM显示出明显的张力发展,伴有叠加在膜电位逐渐下降上的重复电活动。7. 这些结果表明,ACh挛缩主要是由于细胞内储存的Ca释放,而K挛缩主要与细胞外Ca的内流有关。

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