IDENTIFICATION OF PACE-MAKER CURRENT IN FROG ATRIUM

IDENTIFICATION OF PACE-MAKER CURRENT IN FROG ATRIUM
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DOI:
10.1113/jphysiol.1976.sp011434
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发表时间:
1976-01-01
影响因子:
5.5
通讯作者:
NOBLE, SJ
NOBLE, SJ
中科院分区:
医学1区
文献类型:
--
作者:
BROWN, HF;CLARK, A;NOBLE, SJ

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蛙[Rana ridiodea和R. catesbeiana]心房肌进行了研究,使用双蔗糖间隙技术。控制心房起搏器去极化速度的膜电流(起搏器电流,ip)是在正常动作电位的平台电位范围内激活的外向电流。随后在更负的电位下ip失活暴露了非时间依赖性内向膜电流的去极化作用,从而导致起搏电位。通过在诱导起搏器去极化过程中打开电压钳,可以可靠地记录在有限电位范围(约-30 mV至-60 mV)内的ip失活。在更宽的电位范围内研究ip的时间和电压依赖性行为就不那么简单了。描述了在平方电压钳去极化后的衰减尾中,如何将ip与外向电流的其他成分分离。大多数这样的电流衰减尾部包含3个分量的外向电流。看来,这些组件,其中之一是ip,是真正的霍奇金-赫胥黎电导系统主要携带K+。本文还讨论了第三电流的性质,认为它在中等膜电位(约-40 mV)下衰减非常缓慢,是细胞外K+积累的结果。初步证据表明,K+耗竭发生在电位负的小梁的静息电位。
The nature and interactions of the membrane currents underlying induced pace-maker activity in frog [Rana ridibunda and R. catesbeiana] atrial muscle were investigated using a double sucrose gap technique. The membrane current which controls the speed of the atrial pacemaker depolarization (the pace-maker current, ip), was an outward current activated within the plateau potential range of a normal action potential. The subsequent deactivation of ip at more negative potentials unmasked the depolarizing action of time-independent inward membrane currents so that a pace-maker potential can result. The deactivation of ip over a limited potential range (between about -30 and -60 mV) could be reliably recorded by switching on the voltage clamp during an induced pace-maker depolarization. Investigation of the time and voltage-dependent behavior of ip over a much wider potential range was less straightforward. How ip can be separated from other components of outward current present in the decay tails following square voltage clamp depolarizations was described. The majority of such current decay tails contained 3 components of outward current. It appears that 2 of these components, one of which was ip, are true Hodgkin-Huxley conductance systems chiefly carrying K+. The nature of the 3rd current, which decayed very slowly at moderate membrane potentials (about -40 mV), was discussed, and reasons were briefly given for considering it to result from the accumulation of K+ in extracellular spaces. Preliminary evidence that K+ depletion occurs at potentials negative to the resting potential of the trabeculum was also presented.