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蛙心房起搏电流的鉴定。

Identification of the pace-maker current in frog atrium.

作者信息

Brown H F, Clark A, Noble S J

出版信息

J Physiol. 1976 Jul;258(3):521-45. doi: 10.1113/jphysiol.1976.sp011434.

Abstract
  1. The nature and interactions of the membrane currents underlying induced pace-maker activity in frog atrial muscle have been investigated using a double sucrose gap technique. 2. The membrane current which controls the speed of the atrial pacemaker depolarization (the pace-maker current, ip), is shown to be an outward current activated within the plateau potential range of a normal action potential. The subsequent deactivation of ip at more negative potentials unmasks the depolarizing action of time-independent inward membrane currents so that a pace-maker potential can result. 3. The deactivation of ip over a limited potential range (between about -30 and -60 mV) can be reliably recorded by switching on the voltage clamp during an induced pace-maker depolarization. 4. Investigation of the time and voltage-dependent behaviour of ip over a much wider potential range is less straightforward. How ip can be separated from other components of outward current present in the decay tails following square voltage clamp depolarizations is described. 5. The majority of such current decay tails contain three components of outward current. It appears that two of these components, one of which is ip, are true Hodgkin-Huxley conductance systems chiefly carrying potassium ions. 6. The nature of the third current, which decays very slowly at moderate membrane potentials (about -40 mV), is discussed and reasons are briefly given for considering it to result from the accumulation of potassium ions in extracellular spaces. Preliminary evidence that potassium depletion occurs at potentials negative to the resting potential of the trabeculum is also presented. 7. Because of the obvious complexities involved, a quantitative analysis of the atrial outward currents is not attempted here but forms the subject of a following paper (Brown, Clark & Noble, 1976a).
摘要
  1. 利用双蔗糖间隙技术研究了蛙心房肌诱导起搏活动背后的膜电流的性质和相互作用。2. 控制心房起搏去极化速度的膜电流(起搏电流,ip)被证明是一种在正常动作电位的平台期范围内激活的外向电流。随后,ip在更负电位时失活,从而揭示了与时间无关的内向膜电流的去极化作用,进而产生起搏电位。3. 通过在诱导的起搏去极化过程中开启电压钳,可以可靠地记录ip在有限电位范围内(约 -30至 -60 mV之间)的失活情况。4. 在更宽的电位范围内研究ip的时间和电压依赖性行为则不太直接。文中描述了如何将ip与方形电压钳去极化后衰减尾段中存在的外向电流的其他成分分离。5. 大多数此类电流衰减尾段包含三种外向电流成分。其中似乎有两种成分,一种是ip,是主要携带钾离子的真正的霍奇金 - 赫胥黎电导系统。6. 讨论了第三种电流的性质,该电流在中等膜电位(约 -40 mV)下衰减非常缓慢,并简要给出了认为其是由细胞外空间中钾离子积累导致的原因。还提供了小梁电位负于静息电位时发生钾离子耗竭的初步证据。7. 由于涉及明显的复杂性,本文未尝试对心房外向电流进行定量分析,而是将其作为后续论文(Brown, Clark & Noble, 1976a)的主题。

相似文献

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Identification of the pace-maker current in frog atrium.蛙心房起搏电流的鉴定。
J Physiol. 1976 Jul;258(3):521-45. doi: 10.1113/jphysiol.1976.sp011434.
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[Sodium exchange in the atrium of the frog heart].[蛙心心房中的钠交换]
Pflugers Arch Gesamte Physiol Menschen Tiere. 1963;277:36-47.
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