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  Forebrain-specific glutamate receptor B deletion impairs spatial memory but not hippocampal field long-term potentiation

Shimshek, D. R., Jensen, V., Celikel, T., Geng, Y., Schupp, B., Bus, T., et al. (2006). Forebrain-specific glutamate receptor B deletion impairs spatial memory but not hippocampal field long-term potentiation. The Journal of Neuroscience: the Official Journal of the Society for Neuroscience, 26(33), 8428-8440. doi:10.1523/JNEUROSCI.5410-05.2006.

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Item Permalink: http://hdl.handle.net/11858/00-001M-0000-002A-EDC4-0 Version Permalink: http://hdl.handle.net/11858/00-001M-0000-002A-EDC5-E
Genre: Journal Article
Alternative Title : Forebrain specific GluR-B deletion impairs spatial memory but not hippocampal field LTP

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 Creators:
Shimshek, Derya R.1, Author              
Jensen, Vidar, Author
Celikel, Tansu2, Author              
Geng, Yu, Author
Schupp, Bettina1, Author              
Bus, Thorsten3, Author              
Mack, Volker1, Author              
Marx, Verena1, Author              
Hvalby, Øivind, Author
Seeburg, Peter H.1, Author              
Sprengel, Rolf1, Author              
Affiliations:
1Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society, ou_1497704              
2Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society, ou_1497701              
3Max Planck Research Group Behavioural Neurophysiology (Andreas T. Schaefer), Max Planck Institute for Medical Research, Max Planck Society, ou_1497722              

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Free keywords: conditional knock-out; GluR-B; AMPA receptors; LTP; learning and memory; Co2+ uptake; T-maze
 Abstract: We demonstrate the fundamental importance of glutamate receptor B (GluR-B) containing AMPA receptors in hippocampal function by analyzing mice with conditional GluR-B deficiency in postnatal forebrain principal neurons (GluR-B(deltaFb)). These mice are as adults sufficiently robust to permit comparative cellular, physiological, and behavioral studies. GluR-B loss induced moderate long-term changes in the hippocampus of GluR-B(deltaFb) mice. Parvalbumin-expressing interneurons in the dentate gyrus and the pyramidal cells in CA3 were decreased in number, and neurogenesis in the subgranular zone was diminished. Excitatory synaptic CA3-to-CA1 transmission was reduced, although synaptic excitability, as quantified by the lowered threshold for population spike initiation, was increased compared with control mice. These changes did not alter CA3-to-CA1 long-term potentiation (LTP), which in magnitude was similar to LTP in control mice. The altered hippocampal circuitry, however, affected spatial learning in GluR-B(deltaFb) mice. The primary source for the observed changes is most likely the AMPA receptor-mediated Ca2+ signaling that appears after GluR-B depletion, because we observed similar alterations in GluR-B(QFb) mice in which the expression of Ca2+-permeable AMPA receptors in principal neurons was induced by postnatal activation of a Q/R-site editing-deficient GluR-B allele.

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Language(s): eng - English
 Dates: 2006-06-262005-12-192006-06-262006-08-16
 Publication Status: Published in print
 Pages: 13
 Publishing info: -
 Table of Contents: -
 Rev. Method: Peer
 Degree: -

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Title: The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
  Other : J. Neurosci.
Source Genre: Journal
 Creator(s):
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Publ. Info: Baltimore, MD : The Society
Pages: - Volume / Issue: 26 (33) Sequence Number: - Start / End Page: 8428 - 8440 Identifier: ISSN: 0270-6474
CoNE: https://pure.mpg.de/cone/journals/resource/954925502187_1