Na+—Ca2+ Exchange Currents in Cortical Neurons: Concomitant Forward and Reverse Operation and Effect of Glutamate

  title={Na+—Ca2+ Exchange Currents in Cortical Neurons: Concomitant Forward and Reverse Operation and Effect of Glutamate},
  author={Shan Ping Yu and Dennis W. Choi},
  journal={European Journal of Neuroscience},
Na+‐Ca2+ exchanger‐associated membrane currents were studied in cultured murine neocortical neurons, using whole‐cell recording combined with intracellular perfusion. A net inward current specifically associated with forward (Na+o‐Ca2+i) exchange was evoked at ‐40 mV by switching external 140 mM Li+ to 140 mM Na+. The voltage dependence of this current was consistent with that predicted for 3Na+:1Ca2+ exchange. As expected, the current depended on internal Ca2+, and could be blocked by… 
K+‐dependence of Na+–Ca2+ exchange in type I vestibular sensory cells of guinea‐pig
The properties of the vestibular Na+–Ca2+ exchanger in mammalian type I vestibular sensory cells were studied using fura‐2 fluorescence and immunocytochemical techniques. In the absence of external
Na+/Ca2+ exchange and regulation of cytoplasmic concentration of calcium in rat cerebellar neurons treated with glutamate
Reversation of the Na+/Ca2+ exchange reinforced the glutamate-caused perturbations of calcium homeostasis in the neurons and slowed the recovery of the decreased [Ca2-]i in the post-glutamate period.
Differential contribution of plasmalemmal Na+/Ca2+ exchange isoforms to sodium‐dependent calcium influx and NMDA excitotoxicity in depolarized neurons
The data suggest that the high activity of NCX isoforms expressed in FNs, possibly NCX1, sensitizes these neurons to NMDA excitotoxicity.
Reverse Na+/Ca2+ exchange contributes to glutamate-induced intracellular Ca2+ concentration increases in cultured rat forebrain neurons.
Reverse NCE contributes to the immediate rise in [Ca2+]i resulting from glutamate receptor activation, however, reverse NCE becomes less important as the stimulus time is increased, and Ca2+ entry by this route is not critical for the expression of excitotoxic injury.
Sodium/calcium exchange: its physiological implications.
In cardiac myocytes, and probably other cell types, the exchanger serves a housekeeping role by maintaining a low intracellular Ca2+ concentration; its possible role in cardiac excitation-contraction coupling is controversial.
Role of Na+/Ca2+ exchange in [Ca2+]i clearance in rat culture Purkinje neurons requires reevaluation.
It is concluded that the Na(+)/Ca(2+) exchange is strongly suppressed at room temperature and therefore its role should be reevaluated among different neuronal preparations.
A genistein-sensitive Na+/Ca2+ exchange is responsible for the resting [Ca2+]i and most of the Ca2+ plasma membrane fluxes in stimulated rat cerebellar type 1 astrocytes.
In rat cerebellar type 1 astrocytes under resting physiological conditions, most of the total transplasma membrane Ca2+ fluxes take place through the Na+/Ca2+ exchanger, thus accounting for the resting [Ca(2+)]i.
Ca2+ entry through NaV channels generates submillisecond axonal Ca2+ signaling
The findings indicate that Ca2+ permeation through NaV channels provides a submillisecond rapid entry route in NaV-enriched domains of mammalian axons.
Repolarization of the plasma membrane shapes NMDA-induced cytosolic [Ca2+] transients
Monitoring of plasma membrane potential in cultured cerebellar granule cells showed that repolarization of the plasma membrane and inactivation of voltage-gated Ca channels plays the most critical role in restoration of low [Ca2+]c following NMDA receptor inactivation.


Measurement of reversal potential of Na+‐Ca2+ exchange current in single guinea‐pig ventricular cells.
The result indicates that [Ca2+]i, at least under the cell membrane, changes due to ion fluxes through the Na+‐ Ca2+ exchange and that control of the ion concentrations within the cell is prerequisite for measuring the reversal potential of the Na-Ca2- exchange.
Identification of sodium‐calcium exchange current in single ventricular cells of guinea‐pig.
The Na‐Ca exchange current was investigated in single ventricular cells from guinea‐pig hearts by combining the techniques of whole‐cell voltage clamp and intracellular perfusion and showed almost exponential voltage dependence.
Electrogenic Na-Ca exchange clears Ca2+ loads from retinal amacrine cells in culture
Calcium influx into cultured retinal amacrine cells is followed by a small, slow, inward current that is shown to results from the operation of electrogenic Na-Ca exchange, suggesting that variability results from a variable fraction of Ca2+ load, typically 40%, being removed by a process other than Na- Ca exchange.
Sodium-calcium exchange in heart: membrane currents and changes in [Ca2+]i.
Guinea pig ventricular myocytes under voltage clamp were perfused internally with fura-2, a fluorescent Ca2+-indicator, and changes in [Ca2+]i and membrane current that resulted from Na-Ca exchange were identified through the use of various organic channel blockers and impermeant ions.
Perturbation of intracellular calcium and hydrogen ion regulation in cultured mouse hippocampal neurons by reduction of the sodium ion concentration gradient
  • R. Koch, ME Barish
  • Biology
    The Journal of neuroscience : the official journal of the Society for Neuroscience
  • 1994
It is suggested that increased intracellular H+ may synergize with cytoplasmic Ca2+ to potentiate excitotoxic neuronal death during ischemia and hypoglycemia and that Na(+)-H+ exchange limits the acidification (and secondary increase in [Ca2+]i) that accompanies Ca2- influx.
Kinetic properties of the sodium‐calcium exchanger in rat brain synaptosomes.
The symmetry suggests that the voltage‐sensitive step is reversible, and both Ca2P influx and efflux correspond to a Na+‐Ca2+ exchange‐mediated fluxes.
Charge movement during Na+ translocation by native and cloned cardiac Na+/Ca2+ exchanger
It is found that voltage dependence of INaCa in both directions is lost as Ca2+ concentration is decreased and the principal electrogenic step seems to be at the extracellular end of the Na+ translocation pathway.
The Na+‐Ca2+ Exchanger in Rat Brain Synaptosomes
Calcium ions have numerous functions in neurons, including a key role in triggering neurotransmitter release at nerve terminals, and Ca2+ buffering and sequestration may be the main mechanisms for rapidly removing Ca2 from the transmitter releasing sites.
Identification of Na-Ca exchange current in single cardiac myocytes
It is demonstrated that a transient rise in [Ca]i caused by release of Ca from sarcoplasmic reticulum (SR) generates a membrane current in cardiac myocytes, which meets the criteria for a current produced by electrogenic Na-Ca exchange.
Activation of Na-Ca exchange current by photolysis of "caged calcium".