Gleason E, Borges S, Wilson M
Division of Biological Sciences, University of California, Davis 95616, USA.
J Neurosci. 1995 May;15(5 Pt 1):3612-21. doi: 10.1523/JNEUROSCI.15-05-03612.1995.
Calcium influx into cultured retinal amacrine cells is followed by a small, slow, inward current that we show here results from the operation of electrogenic Na-Ca exchange. The activity of the exchanger is shown to correlate with the magnitude of the Ca2+ load and to depend on both the Ca2+ and Na+ gradients. Li+ is unable to substitute for Na+ and in the absence of Na+, slow tail currents are almost entirely suppressed. A rapid change in [K+]o does not affect the activity of the exchanger, suggesting that only Na+ and Ca2+ are transported. The ratio of charge entering as Ca2+ current to the charge entering as exchange current is highly variable between cells. We suggest that variability results from a variable fraction of Ca2+ load, we estimate typically 40%, being removed by a process other than Na-Ca exchange. This process is likely to involve internal buffering or sequestration since inhibition of the plasmalemmal Ca(2+)-ATPase does not increase the fraction of Ca2+ expelled by the exchanger. Ca2+ loading performed in the absence of Na+o generates smaller exchange charge the longer the delay in returning Na+o to the neuron. About 30% of exchange charge is lost for a delay of 1 sec.
钙离子流入培养的视网膜无长突细胞后，会伴随一个小的、缓慢的内向电流，我们在此表明，该电流是由电致钠钙交换的运作产生的。已证明交换器的活性与Ca2+负荷的大小相关，并取决于Ca2+和Na+梯度。Li+不能替代Na+，在没有Na+的情况下，缓慢的尾电流几乎完全被抑制。细胞外[K+]的快速变化不会影响交换器的活性，这表明只有Na+和Ca2+被转运。作为Ca2+电流进入的电荷与作为交换电流进入的电荷之比在不同细胞之间高度可变。我们认为，这种变异性是由于可变比例的Ca2+负荷（我们估计通常为40%）通过钠钙交换以外的过程被清除。这个过程可能涉及内部缓冲或螯合，因为抑制质膜Ca(2+)-ATP酶不会增加交换器排出的Ca2+比例。在没有细胞外Na+的情况下进行Ca2+加载，细胞外Na+返回神经元的延迟时间越长，产生的交换电荷就越小。延迟1秒会损失约30%的交换电荷。
