Intracellular calcium elevation during plateau potentials mediated by extrasynaptic NMDA receptor activation in rat hippocampal CA1 pyramidal neurons is primarily due to calcium entry through voltage‐gated calcium channels. (27th March 2014)

• Record Type: Journal Article
• Authors: Oda, Yoshiaki; Kodama, Satoshi; Tsuchiya, Sadahiro; Inoue, Masashi; Miyakawa, Hiroyoshi
• Is Part Of: European journal of neuroscience. Volume 39:Number 10(2014:May)
• Page Start: 1613
• Page End: 1623
• Publication Date: 2014-03-27
• Subjects: Nervous system -- Periodicals; 612.8
• DOI: 10.1111/ejn.12555
• Languages: English
• ISSNs: 0953-816X

Abstract

<abstract abstract-type="main" id="ejn12555-abs-0001"> <title>Abstract</title> <p>We reported previously that plateau potentials mediated by extrasynaptic <italic>N</italic>‐methyl‐<sc>d</sc>‐aspartate receptors (NMDARs) can be induced either by synaptic stimulation in the presence of glutamate transporter antagonist or by iontophoresis of NMDA in rat hippocampal CA1 pyramidal neurons. To examine whether the plateau potentials are accompanied by an elevation of intracellular Ca<sup>2+</sup> and to determine the source of Ca<sup>2+</sup> elevation, we performed Ca<sup>2+</sup> imaging during the plateau potential. Neurons were loaded with Ca<sup>2+</sup> indicator fluo‐4, and the plateau potentials were generated either synaptically in the presence of glutamate transporter antagonist or by iontophoretically applying NMDA. We have found that a transient elevation in intracellular Ca<sup>2+</sup> accompanies the plateau potential. The synaptically induced plateau potential and the Ca<sup>2+</sup> elevation were blocked by 5, 7‐dichlorokynurenic acid (5, 7‐dCK), an antagonist for the glycine‐binding sites of NMDAR. A mixture of Cd<sup>2+</sup> and tetrodotoxin did not block NMDA‐induced plateau potentials, but completely abolished the accompanying Ca<sup>2+</sup> elevation in both the presence and absence of Mg<sup>2+</sup> ions in the bathing solution. The NMDA‐induced plateau potential was blocked by further adding 5, 7‐dCK. Our results show that the NMDAR‐mediated plateau potential is accompanied by elevation of intracellular Ca<sup>2+</sup> that is primarily caused by the influx of Ca<sup>2+</sup> through voltage‐gated Ca<sup>2+</sup> channels.</p> </abstract>