Key result
NCKX-mediated Ca2+ influx proceeds several times faster in CA1 neurons versus forebrain cells, resisting inhibitors.
The significantly higher rate of NCKX-mediated Ca2+ influx in CA1 neurons may contribute to their specific vulnerability to ischemic death.
Ca(2+) influx via reversed K(+)-dependent (NCKX) and/or K(+)-independent (NCX) plasmalemmal Na(+)/Ca(2+) exchangers may play a role in neuronal death following global brain ischemia to which CA1 neurons are particularly vulnerable. Therefore, this work tested whether the rates of Ca(2+) influx via reversed NCKX or NCX in cultured rat CA1 neurons differ from those in forebrain neurons (FNs) or cerebellar granule cells (CGCs). The NCKX-mediated Ca(2+) influx was several times more rapid in CA1 neurons than in FNs or CGCs and was not affected by Na(+)/Ca(2+) exchange inhibitors, KB-R7943 or bepridil. NCKX reversal inhibitors are not yet available. Their development would greatly facilitate further testing the role of NCKX in ischemic death of CA1 neurons.
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Lech Kiedrowski (2004) studied Global brain ischemia. NCKX-mediated Ca2+ influx vs. Forebrain neurons or cerebellar granule cells was evaluated on Rates of Ca2+ influx via reversed NCKX or NCX. NCKX-mediated Ca2+ influx was several times more rapid in cultured rat CA1 neurons than in forebrain neurons or cerebellar granule cells, and was unaffected by Na+/Ca2+ exchange inhibitors.
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