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大鼠肌肉中内源性稳定电流的特性。

Properties of an endogenous steady current in rat muscle.

作者信息

Caldwell J H, Betz W J

出版信息

J Gen Physiol. 1984 Feb;83(2):157-73. doi: 10.1085/jgp.83.2.157.

Abstract

A vibrating probe was used to study a steady electric current generated by isolated, whole lumbrical muscles of the rat. Spatial mapping showed that current leaves the muscle in the synaptic region and re-enters in the flanking extrajunctional regions. The point of maximum outward current coincided precisely with the endplate region. As the probe was moved radially away from the endplate region, the current declined monotonically, and the results could be fit with a simple model. As the probe was moved axially away from the endplate region, the current declined and became inward over a distance of approximately 0.5 mm. The physiological mechanism by which the current is generated was also studied. alpha-Bungarotoxin and tetrodotoxin had no significant effect on the current, which suggests that acetylcholine channels and gated sodium channels are not involved in the generation of the current. Ouabain produced a slowly developing, partial inhibition of the current, reducing it by approximately 40% over a period of 30-40 min. Carbachol produced a large inward current at the endplate region. After the carbachol action was terminated with alpha-bungarotoxin, an outward current reappeared, and a transient "overshoot" developed. During the overshoot, which lasted approximately 30-40 min, the outward current was approximately doubled. This overshoot was completely abolished by ouabain. The overshoot is interpreted as reflecting the increased activity of electrogenic sodium pumping in the endplate region, caused by the influx of Na ions during carbachol application. Because of the very different actions of ouabain on the normal current and on the overshoot after carbachol application, we concluded that the normal outward current is not produced by electrogenic sodium pumping in the endplate region.

摘要

使用振动探针研究大鼠离体完整蚓状肌产生的稳定电流。空间映射显示电流在突触区域离开肌肉,并在相邻的结外区域重新进入。最大外向电流点与终板区域精确重合。随着探针从终板区域径向移开,电流单调下降,结果可以用一个简单模型拟合。随着探针从终板区域轴向移开,电流下降并在大约0.5毫米的距离内变为内向。还研究了产生电流的生理机制。α-银环蛇毒素和河豚毒素对电流没有显著影响,这表明乙酰胆碱通道和门控钠通道不参与电流的产生。哇巴因对电流产生缓慢发展的部分抑制作用,在30 - 40分钟内使其降低约40%。卡巴胆碱在终板区域产生大的内向电流。在用α-银环蛇毒素终止卡巴胆碱作用后,外向电流重新出现,并出现短暂的“过冲”。在持续约30 - 40分钟的过冲期间,外向电流大约加倍。这种过冲被哇巴因完全消除。过冲被解释为反映了在卡巴胆碱应用期间钠离子内流导致终板区域电生钠泵活性增加。由于哇巴因对正常电流和卡巴胆碱应用后的过冲有非常不同的作用,我们得出结论,正常的外向电流不是由终板区域的电生钠泵产生的。

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