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The Journal of Neuroscience, August 16, 2006, 26(33):8428-8440; doi:10.1523/JNEUROSCI.5410-05.2006

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Behavioral/Systems/Cognitive
Forebrain-Specific Glutamate Receptor B Deletion Impairs Spatial Memory But Not Hippocampal Field Long-Term Potentiation

Derya R. Shimshek,¹ Vidar Jensen,³ Tansu Celikel,² Yu Geng,¹ Bettina Schupp,¹ Thorsten Bus,¹ Volker Mack,¹ Verena Marx,¹ Øivind Hvalby,³ Peter H. Seeburg,¹ and Rolf Sprengel¹

Departments of ¹Molecular Neurobiology and ²Cell Physiology, Max Planck Institute for Medical Research, D-69120 Heidelberg, Germany, and ³Molecular Neurobiology Research Group, Institute of Basic Medical Sciences, University of Oslo, N-0317 Oslo, Norway

Correspondence should be addressed to Rolf Sprengel, Max Planck Institute for Medical Research, Jahnstrasse 29, D-69120 Heidelberg, Germany. Email: sprengel{at}mpimf-heidelberg.mpg.de

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^Fb). 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^Fb 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^Fb 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.

Key words: conditional knock-out; GluR-B; AMPA receptors; LTP; learning and memory; Co²⁺ uptake; T-maze

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Received Dec. 19, 2005; revised June 26, 2006; accepted June 26, 2006.

Correspondence should be addressed to Rolf Sprengel, Max Planck Institute for Medical Research, Jahnstrasse 29, D-69120 Heidelberg, Germany. Email: sprengel{at}mpimf-heidelberg.mpg.de

This article has been cited by other articles:

				S. Panicker, K. Brown, and R. A. Nicoll Synaptic AMPA receptor subunit trafficking is independent of the C terminus in the GluR2-lacking mouse PNAS, January 22, 2008; 105(3): 1032 - 1037. [Abstract] [Full Text] [PDF]

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