Na+/Ca2+ exchange, Na+−K+ pump and a delayed glutamate neurotoxicity

Role of Na+/Ca2+ exchange in regulation of neuronal Ca2+ homeostasis requires re‐evaluation

“…Addition of AP‐5 abolished the effect of Na + o removal indicating that at high pH o , as well as at pH o 7.4, the CaR mainly resulted from the Ca 2+ influx via NMDA channels. An increase in the amplitude of the CaR at pH o 8.5 can be readily explained by the fact that pH o elevation potentiated the agonist‐induced activation of NMDA channels [10]along with suppression of the Ca 2+ /H + pump‐mediated Ca 2+ extrusion from the cell [11]. Note that AP‐5 did not prevent [Ca 2+ ] i elevation induced by high pH o .…”

Li+ protects nerve cells against destabilization of Ca2+ homeostasis and delayed death caused by removal of external Na+

“…It is established, however, that both the Na + /Ca 2+ exchange and Na + ‐dependent Glu transport can be also reversed by the Na + /Li + substitution [1, 2, 4]. Meanwhile in nerve cells this replacement produces only a very small deregulation of [Ca 2+ ] i homeostasis as compared to that caused by Na + /NMDG replacement [6, 7]. The aim of the present study was to clarify the reason for this surprising difference between the effects of external Na + substitution with NMDG and Li + on neuronal [Ca 2+ ] i homeostasis.…”