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The Journal of Neuroscience, July 20, 2005, 25(29):6907-6910; doi:10.1523/JNEUROSCI.1905-05.2005
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BRIEF COMMUNICATION
Lack of NMDA Receptor Subtype Selectivity for Hippocampal Long-Term Potentiation
Sven Berberich,1 * Pradeep Punnakkal,1 * Vidar Jensen,2 Verena Pawlak,1 Peter H. Seeburg,1 Øivind Hvalby,2 andGeorg Köhr1 1Department of Molecular Neurobiology, Max-Planck-Institute for Medical Research, D-69120 Heidelberg, Germany, and 2Molecular Neurobiology Research Group, Institute of Basic Medical Sciences, University of Oslo, N-0317 Oslo, Norway
NMDA receptor (NMDAR) 2A (NR2A)- and NR2B-type NMDARs coexist in synapses of CA1 pyramidal cells. Recent studies using pharmacological blockade of NMDAR subtypes proposed that the NR2A type is responsible for inducing long-term potentiation (LTP), whereas the NR2B type induces long-term depression (LTD). This contrasts with the finding in genetically modified mice that NR2B-type NMDARs induce LTP when NR2A signaling is absent or impaired, although compensatory mechanisms might have contributed to this result. We therefore assessed the contribution of the two NMDAR subtypes to LTP in mouse hippocampal slices by different induction protocols and in the presence of NMDAR antagonists, including the NR2A-type blocker NVP-AAM077, for which an optimal concentration for subtype selectivity was determined on recombinant and native NMDARs. Partial blockade of NMDA EPSCs by 40%, either by preferentially antagonizing NR2A- or NR2B-type NMDARs or by the nonselective antagonist D-AP-5, did not impair LTP, demonstrating that hippocampal LTP induction can be generated by either NMDAR subtype.
Key words: NVP-AAM077; PEAQX; CP-101,606; recombinant; gene-targeted mouse; partial blockade; pairing
Received May 12, 2005; revised June 15, 2005; accepted June 16, 2005.
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