title: Cellular prion protein null mice display normal AMPA receptor mediated long term depression.
abstract: Cellular prion protein (PrP(C)) appears to be involved in numerous physiological processes. We have recently shown a novel modulation of NMDA receptors by PrP(C) that results in neuroprotection via silencing of NMDA receptors containing NR2D subunits, whereas no effects on AMPA receptor function could be observed (Khosravani, et al. J Cell Biol 2008; 181:551). Here we show that PrP-null mice show a normal response to long-term depression stimuli requiring AMPA receptor activity, thus further supporting our previous findings of a selective action on NMDA receptors among ionotropic glutamate receptors.
authors.affiliation: Department of Physiology and Biophysics, Hotchkiss Brain Institute, University of Calgary, Calgary, Canada.
authors.forename: Houman
authors.initials: H
authors.lastname: Khosravani
authors.forename: Yunfeng
authors.initials: Y
authors.lastname: Zhang
authors.forename: Gerald W
authors.initials: GW
authors.lastname: Zamponi
mesh_terms: D000818:Animals; D020868:Gene Silencing; D051379:Mice; D018345:Mice, Knockout; D018621:PrPC Proteins / Q000235:genetics / Q000378:metabolism*; D017096:Prion Diseases / Q000235:genetics / Q000378:metabolism*; D018091:Receptors, AMPA / Q000235:genetics / Q000378:metabolism*; D016194:Receptors, N-Methyl-D-Aspartate / Q000235:genetics / Q000378:metabolism*
chemical_list: C464436:NR2D NMDA receptor; D018621:PrPC Proteins; D018091:Receptors, AMPA; D016194:Receptors, N-Methyl-D-Aspartate