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膜极化对骨骼肌纤维收缩阈值及延长收缩反应时间进程的影响。

Effect of membrane polarization on contractile threshold and time course of prolonged contractile responses in skeletal muscle fibers.

作者信息

Caputo C, Bolaños P, Gonzalez G F

出版信息

J Gen Physiol. 1984 Dec;84(6):927-43. doi: 10.1085/jgp.84.6.927.

Abstract

Short muscle fibers (less than 1.5 mm) from the m. lumbricalis IV digiti of Rana pipiens were voltage-clamped at -100 mV with a two-microelectrode technique, in normal Ringer's solution containing 10(-6) g/ml tetrodotoxin. The activation curve relating peak tension to membrane potential could be shifted toward more negative or less negative potential values by hyperpolarizing or depolarizing the fiber membrane to -130, -120, or -70 mV, respectively, which indicates that contractile threshold depends on the fiber membrane potential. Long (greater than 5 s) depolarizing (90 mV) pulses induce prolonged contractile responses showing a plateau and a rapid relaxation phase similar to K contractures. Conditioning hyperpolarizations prolong the time course of these responses, while conditioning depolarizations shorten it. The shortening of the response time course, which results in a decrease of the area under the response, is dependent on the amplitude and duration of the conditioning depolarization. Depending on the magnitude and duration, a conditioning depolarization may also reduce peak tension. When the area under the response is reduced by 50%, the level of membrane potential also affects the repriming rate. During repriming, peak tension is restored before the contracture area. Thus, when peak tension is reprimed to 80%, the area is reprimed by 50% of its normal value. Repriming has a marked temperature dependency with a Q10 higher than 4. These results are compatible with the idea that an inactivation process, voltage and time dependent, regulates the release of calcium from the sarcoplasmic reticulum during these responses.

摘要

用双微电极技术,在含有10(-6)克/毫升河豚毒素的正常林格氏液中,将牛蛙第四蚓状肌的短肌纤维(小于1.5毫米)电压钳制在-100毫伏。通过分别将纤维膜超极化或去极化至-130、-120或-70毫伏,可使将峰值张力与膜电位相关的激活曲线向更负或更不负的电位值移动,这表明收缩阈值取决于纤维膜电位。长时间(大于5秒)的去极化(90毫伏)脉冲会诱发延长的收缩反应,呈现出一个平台期和一个类似于钾挛缩的快速松弛期。预处理超极化会延长这些反应的时间进程,而预处理去极化则会缩短它。反应时间进程的缩短,导致反应下面积减小,这取决于预处理去极化的幅度和持续时间。根据幅度和持续时间的不同,预处理去极化也可能降低峰值张力。当反应下面积减少50%时,膜电位水平也会影响再激发率。在再激发过程中,峰值张力在挛缩面积恢复之前恢复。因此,当峰值张力再激发到80%时,则面积再激发到其正常值的50%。再激发具有明显的温度依赖性,Q10高于4。这些结果与这样一种观点相符,即在这些反应过程中,一个电压和时间依赖性的失活过程调节着肌浆网中钙的释放。

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