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  Frequency dependent impairment of hippocampal LTP from NMDA receptors with reduced calcium permeability

Pawlak, V., Jensen, V., Schupp, B., Kvello, A., Hvalby, Ø., Seeburg, P. H., et al. (2005). Frequency dependent impairment of hippocampal LTP from NMDA receptors with reduced calcium permeability. European Journal of Neuroscience: European Neuroscience Association, 22(2), 476-484. doi:10.1111/j.1460-9568.2005.04226.x.

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Item Permalink: http://hdl.handle.net/11858/00-001M-0000-002A-C518-8 Version Permalink: http://hdl.handle.net/11858/00-001M-0000-002A-C519-6
Genre: Journal Article
Alternative Title : Frequency dependent impairment of hippocampal LTP from NMDA receptors with reduced calcium permeability

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EurJNeurosci_22_2005_476.pdf (Any fulltext), 281KB
 
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 Creators:
Pawlak, Verena1, 2, Author              
Jensen, Vidar, Author
Schupp, Bettina2, Author              
Kvello, Ane, Author
Hvalby, Øivind, Author
Seeburg, Peter H.2, Author              
Köhr, Georg2, Author              
Affiliations:
1Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society, ou_1497701              
2Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society, ou_1497704              

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Free keywords: CA3-to-CA1 synapse; gene-targeted mouse; pairing; point mutation; tetanic stimulation
 Abstract: Changes in postsynaptic Ca2+ levels are essential for alterations in synaptic strength. At hippocampal CA3-to-CA1 synapses, the Ca2+ elevations required for LTP induction are typically mediated by NMDA receptor (NMDAR) channels but a contribution of NMDAR-independent Ca2+ sources has been implicated. Here, we tested the sensitivity of different protocols modifying synaptic strength to reduced NMDAR-mediated Ca2+ influx by employing mice genetically programmed to express in forebrain principal neurons an NR1 form that curtails Ca2+ permeability. Reduced NMDAR-mediated Ca2+ influx did not facilitate synaptic depression in CA1 neurons of these genetically modified mice. However, we observed that LTP could not be induced by pairing low frequency synaptic stimulation (LFS pairing) with postsynaptic depolarization, a protocol that induced robust LTP in wild-type mice. By contrast to LFS pairing, similar LTP levels were generated in both genotypes when postsynaptic depolarization was paired with high frequency synaptic stimulation (HFS). This indicates that the postsynaptic Ca2+ elevation also reached threshold during HFS in the mutant, probably due to summation of NMDAR-mediated Ca2+ influx. However, only in wild-type mice did repeated HFS further enhance LTP. All tested forms of LTP were blocked by the NMDAR antagonist D-AP5. Collectively, our results indicate that only NMDAR-dependent Ca2+ sources (NMDARs and Ca2+-dependent Ca2+ release from intracellular stores) mediate LFS pairing-evoked LTP. Moreover, LTP induced by the first HFS stimulus train required lower Ca2+ levels than the additional LTP obtained by repeated trains.

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Language(s): eng - English
 Dates: 2005-04-272005-01-062005-05-162005-07-01
 Publication Status: Published in print
 Pages: 9
 Publishing info: -
 Table of Contents: -
 Rev. Type: Peer
 Degree: -

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Title: European Journal of Neuroscience : European Neuroscience Association
  Other : Eur. J. Neurosci
Source Genre: Journal
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Publ. Info: Oxford, UK : Published on behalf of the European Neuroscience Association by Oxford University Press
Pages: - Volume / Issue: 22 (2) Sequence Number: - Start / End Page: 476 - 484 Identifier: ISSN: 0953-816X
CoNE: https://pure.mpg.de/cone/journals/resource/954925575988