Differential calcium-dependent modulation of NMDA currents in CA1 and CA3 hippocampal pyramidal cells

Grishin, Anton A., Gee, Christine E., Gerber, Urs and Benquet, Pascal (2004) Differential calcium-dependent modulation of NMDA currents in CA1 and CA3 hippocampal pyramidal cells. Journal of Neuroscience, 24 2: 350-355. doi:10.1523/JNEUROSCI.4933-03.2004

Attached Files (Some files may be inaccessible until you login with your UQ eSpace credentials)
Name Description MIMEType Size Downloads
UQ122913_OA.pdf Full text (open access) application/pdf 269.54KB 0

Author Grishin, Anton A.
Gee, Christine E.
Gerber, Urs
Benquet, Pascal
Title Differential calcium-dependent modulation of NMDA currents in CA1 and CA3 hippocampal pyramidal cells
Journal name Journal of Neuroscience   Check publisher's open access policy
ISSN 0270-6474
1529-2401
Publication date 2004
Sub-type Article (original research)
DOI 10.1523/JNEUROSCI.4933-03.2004
Open Access Status File (Publisher version)
Volume 24
Issue 2
Start page 350
End page 355
Total pages 6
Place of publication Washington
Publisher Soc Neuroscience
Language eng
Abstract Neuronal Ca2+ influx via NMDA receptors (NMDARs) is essential for the development and plasticity of synapses but also triggers excitotoxic cell death when critical intracellular levels are exceeded. Therefore, finely equilibrated mechanisms are necessary to ensure that NMDAR function is maintained within a homeostatic range. Here we describe a pronounced difference in the modulation of NMDA currents in two closely related hippocampal cell types, the CA1 and the CA3 pyramidal cells (PCs). Manipulations that increase intracellular Ca2+ levels strongly depressed NMDA currents in CA3 with only minor effects in CA1 PCs. Furthermore, activation of G(q)-coupled metabotropic receptors potentiated NMDA currents in CA1 PCs but depressed them in CA3 PCs. Interestingly, the CA3 type modulation of NMDARs could be converted into CA1-like behavior, and vice versa, by increasing Ca2+ buffering in CA3 cells or decreasing Ca2+ buffering in CA1 cells, respectively. Our data suggest that a differential Ca2+ sensitivity of the regulatory cascades targeting NMDARs plays a key role in determining the direction and magnitude of NMDA responses in various types of neurons. These findings may have important implications for NMDA receptor-dependent synaptic plasticity and the differential sensitivity of CA1 and CA3 PCs to NMDAR-dependent ischemic cell death.
Keyword Neurosciences
acetylcholine
ACh
depression
muscarinic
potentiation
glutamate
metabotropic glutamate receptor
Metabotropic Glutamate Receptors
Protein-kinase-c
Excitatory Synaptic-transmission
Tyrosine Phosphatase Step
Rat Hippocampus
Selective Vulnerability
Potentiation
Activation
Subunits
Neurons
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Unknown

Document type: Journal Article
Sub-type: Article (original research)
Collections: Excellence in Research Australia (ERA) - Collection
School of Biomedical Sciences Publications
 
Versions
Version Filter Type
Citation counts: TR Web of Science Citation Count  Cited 29 times in Thomson Reuters Web of Science Article | Citations
Scopus Citation Count Cited 34 times in Scopus Article | Citations
Google Scholar Search Google Scholar
Created: Fri, 25 Jan 2008, 16:05:51 EST