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Updated: Aug 1, 2026

Multi-photon Intracellular Sodium Imaging Combined with UV-mediated Focal Uncaging of Glutamate in CA1 Pyramidal Neurons
Published on: October 8, 2014
Repolarization of the plasma membrane shapes NMDA-induced cytosolic [Ca2+ ] transients
1The 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.
Abstract:
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.
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