TY - JOUR T1 - Forebrain-Specific Glutamate Receptor B Deletion Impairs Spatial Memory But Not Hippocampal Field Long-Term Potentiation JF - The Journal of Neuroscience JO - J. Neurosci. SP - 8428 LP - 8440 DO - 10.1523/JNEUROSCI.5410-05.2006 VL - 26 IS - 33 AU - Derya R. Shimshek AU - Vidar Jensen AU - Tansu Celikel AU - Yu Geng AU - Bettina Schupp AU - Thorsten Bus AU - Volker Mack AU - Verena Marx AU - Øivind Hvalby AU - Peter H. Seeburg AU - Rolf Sprengel Y1 - 2006/08/16 UR - http://www.jneurosci.org/content/26/33/8428.abstract N2 - 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-BΔFb). 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-BΔFb 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-BΔFb 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-BQFb 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. ER -