Friedman A, Arens J, Heinemann U, Gutnick M J
Department of Physiology, Corob Center for Medical Research, Faculty of Health Sciences, Ben Gurion University of the Negev, Beersheva, Israel.
Neurosci Lett. 1992 Jan 20;135(1):13-7. doi: 10.1016/0304-3940(92)90125-q.
Depolarizing afterpotentials (DAPs) were studied in intracellular recordings from neocortical slices bathed in tetrodotoxin (TTX) (1 microM) and tetraethylammonium chloride (TEA) (24 mM), to block voltage-dependent Na+ currents and most K+ currents. The DAP was Ca(2+)-dependent, in that its magnitude varied as a function of the duration of the preceding Ca2+ plateau. It had an apparent reversal potential of between -40 and -5 mV. The DAP was blocked when choline replaced all extracellular Na+; there was a hyperpolarizing shift in apparent reversal potential when extracellular Na+ was lowered. The DAP was blocked by amiloride (1 mM), which also decreased the preceding Ca2+ plateau. The data are consistent with the hypothesis that the DAP is due to electrogenic Na+/Ca2+ exchange.
在浸泡于河豚毒素(TTX)(1微摩尔)和四乙铵氯化物(TEA)(24毫摩尔)中的新皮质切片的细胞内记录中研究了去极化后电位(DAPs),以阻断电压依赖性Na +电流和大多数K +电流。DAP是Ca(2+)依赖性的,其幅度随前一个Ca2 +平台期的持续时间而变化。它的表观反转电位在-40至-5毫伏之间。当胆碱取代所有细胞外Na +时,DAP被阻断;当细胞外Na +降低时,表观反转电位出现超极化偏移。DAP被氨氯地平(1毫摩尔)阻断,氨氯地平也降低了前一个Ca2 +平台期。这些数据与DAP是由于电生Na + / Ca2 +交换的假设一致。