Repolarization of the plasma membrane shapes NMDA-induced cytosolic [Ca2+ ] transients.
After inactivation of NMDA receptors, restoration of basal cytosolic [Ca2+] ([Ca2+]c) is delayed. This may be caused by Ca2+ influx via reverse Na/Ca exchange or voltage-gated Ca2+ channels, and/or by Ca2+ efflux from internal stores. Monitoring of [Na+]c, [Ca2+]c, and 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. During NMDA receptor activation, however, an Na-dependent mechanism enhanced NMDA-induced elevation in [Ca2+]c. This mechanism did not involve Na,K-ATPase activation by Na+, because it operated even when Na,K-ATPase was inhibited.
Kiedrowski
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The Psychiatric Institute, Department of Psychiatry and Pharmacology, College of Medicine, University of Illinois at Chicago, 1601 W. Taylor Street, Room 334W, Chicago, IL 60612, USA.
D000818:Animals; D000831:Animals, Newborn; D002118:Calcium / Q000378:metabolism*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000378:metabolism*; D002413:Cations, Divalent; D002462:Cell Membrane / Q000187:drug effects / Q000378:metabolism; D002478:Cells, Cultured; D002531:Cerebellum / Q000187:drug effects / Q000378:metabolism; D003600:Cytosol / Q000187:drug effects / Q000378:metabolism; D004791:Enzyme Inhibitors / Q000494:pharmacology; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D009474:Neurons / Q000187:drug effects / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D016194:Receptors, N-Methyl-D-Aspartate / Q000037:antagonists & inhibitors* / Q000378:metabolism
D002121:Calcium Channel Blockers; D015220:Calcium Channels; D002413:Cations, Divalent; D004791:Enzyme Inhibitors; D016194:Receptors, N-Methyl-D-Aspartate; D002118:Calcium