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Identification of the pace-maker current in frog atrium.

机译:识别蛙心房中的起搏器电流。

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摘要

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).
机译:1.使用双蔗糖间隙技术研究了青蛙心房中引起起搏器活动的膜电流的性质和相互作用。 2.控制心房起搏器去极化速度的膜电流(起搏器电流,ip)显示为在正常动作电位的平台电位范围内激活的向外电流。随后在更多负电势下的ip失活掩盖了与时间无关的内向膜电流的去极化作用,因此可以产生起搏器电势。 3.通过在感应起搏器去极化过程中接通电压钳,可以可靠地记录ip在有限电位范围内的失活(约-30至-60 mV)。 4.在更宽的电位范围内研究ip的时间和电压相关行为并不那么简单。描述了如何在平方电压钳位去极化之后将ip与衰减尾部中存在的向外电流的其他分量分离。 5.大多数此类电流衰减尾部包含向外电流的三个分量。这些成分中有两个似乎是ip,它们是真正的霍奇金-赫克斯利电导系统,主要携带钾离子。 6.讨论了第三电流的性质,该电流在中等膜电位(约-40 mV)下衰减非常缓慢,并简要说明了考虑第三势由钾离子在细胞外空间积聚而产生的原因。初步证据表明钾耗竭发生在对小梁的静息电位负的电位。 7.由于涉及的明显复杂性,此处未尝试对心房外向流进行定量分析,而是构成了后续论文的主题(Brown,Clark和Noble,1976a)。

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