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). ⋯ NCKX reversal inhibitors are not yet available. Their development would greatly facilitate further testing the role of NCKX in ischemic death of CA1 neurons.
The Psychiatric Institute, Departments of Psychiatry and Pharmacology, University of Illinois at Chicago, 1601 W. Taylor St., Chicago, IL 60612, USA. Lkiedr@psych.uicedu
Neuroreport. 2004 Sep 15; 15 (13): 2113-6.
AbstractCa(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.