English
 
Help Privacy Policy Disclaimer
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT

Released

Journal Article

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

MPS-Authors
/persons/resource/persons95339

Shimshek,  Derya R.
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

/persons/resource/persons92449

Celikel,  Tansu
Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society;

/persons/resource/persons95249

Schupp,  Bettina
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

/persons/resource/persons92385

Bus,  Thorsten
Max Planck Research Group Behavioural Neurophysiology (Andreas T. Schaefer), Max Planck Institute for Medical Research, Max Planck Society;

/persons/resource/persons94171

Mack,  Volker
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

/persons/resource/persons123282

Marx,  Verena
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

/persons/resource/persons95292

Seeburg,  Peter H.
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

/persons/resource/persons95439

Sprengel,  Rolf
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

Fulltext (restricted access)
There are currently no full texts shared for your IP range.
Fulltext (public)
There are no public fulltexts stored in PuRe
Supplementary Material (public)
There is no public supplementary material available
Citation

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.


Cite as: https://hdl.handle.net/11858/00-001M-0000-002A-EDC4-0
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.