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Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-148

Grishin, A A; Gee, C E; Gerber, U; Benquet, P (2004). Differential calcium-dependent modulation of NMDA currents in CA1 and CA3 hippocampal pyramidal cells. Journal of Neuroscience, 24(2):350-355.

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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.


29 citations in Web of Science®
32 citations in Scopus®
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54 downloads since deposited on 11 Feb 2008
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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > Brain Research Institute
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Deposited On:11 Feb 2008 12:13
Last Modified:05 Apr 2016 12:12
Publisher:Society for Neuroscience
Additional Information:Holder of copyright: The Society for Neuroscience
Publisher DOI:10.1523/JNEUROSCI.4933-03.2004
PubMed ID:14724233

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