Russell J M, Brown A M
J Gen Physiol. 1972 Nov;60(5):499-518. doi: 10.1085/jgp.60.5.499.
Internal chloride activity, a(i) (Cl), and membrane potential, E(m), were measured simultaneously in 120 R2 giant neurons of Aplysia californica. a(i) (Cl) was 37.0 +/- 0.8 mM, E(m) was -49.3 +/- 0.4 mv, and E(Cl) calculated using the Nernst equation was -56.2 +/- 0.5 mv. Such values were maintained for as long as 6 hr of continuous recording in untreated neurons. Cooling to 1 degrees -4 degrees C caused a(i) (Cl) to increase at such a rate that 30-80 min after cooling began, E(Cl) equalled E(m). The two then remained equal for as long as 6 hr. Rewarming to 20 degrees C caused a(i) (Cl) to decline, and E(Cl) became more negative than E(m) once again. Exposure to 100 mM K(+)-artificial seawater caused a rapid increase of a(i) (Cl). Upon return to control seawater, a(i) (Cl) declined despite an unfavorable electrochemical gradient and returned to its control values. Therefore, we conclude that chloride is actively transported out of this neuron. The effects of ouabain and 2,4-dinitrophenol were consistent with a partial inhibitory effect. Chloride permeability calculated from net chloride flux using the constant field equation ranged from 4.0 to 36 x 10(-8) cm/sec.
在120个加州海兔的R2巨型神经元中同时测量了细胞内氯离子活性a(i)(Cl)和膜电位E(m)。a(i)(Cl)为37.0±0.8 mM,E(m)为-49.3±0.4 mV,使用能斯特方程计算出的E(Cl)为-56.2±0.5 mV。在未处理的神经元中,这样的值在长达6小时的连续记录中保持稳定。冷却至1℃-4℃会使a(i)(Cl)以一定速率增加,以至于在冷却开始后30-80分钟,E(Cl)等于E(m)。然后两者在长达6小时内保持相等。重新升温至20℃会使a(i)(Cl)下降,E(Cl)再次变得比E(m)更负。暴露于100 mM K(+)-人工海水中会使a(i)(Cl)迅速增加。回到对照海水后,尽管存在不利的电化学梯度,a(i)(Cl)仍会下降并恢复到其对照值。因此,我们得出结论,氯离子被主动转运出该神经元。哇巴因和2,4-二硝基苯酚的作用与部分抑制作用一致。使用恒定场方程根据净氯离子通量计算出的氯离子渗透率范围为4.0至36×10(-8) cm/秒。