D
Derek Bowie
Researcher at McGill University
Publications - 69
Citations - 7602
Derek Bowie is an academic researcher from McGill University. The author has contributed to research in topics: Kainate receptor & AMPA receptor. The author has an hindex of 25, co-authored 63 publications receiving 7149 citations. Previous affiliations of Derek Bowie include Université de Montréal & National Institutes of Health.
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Journal Article
The glutamate receptor ion channels
TL;DR: The cloning of cDNAs encoding glutamate receptor subunits, which occurred mainly between 1989 and 1992, stimulated the development of ionotropic glutamate receptors in the brain.
Journal ArticleDOI
Control of GluR1 AMPA Receptor Function by cAMP-Dependent Protein Kinase
Tue G. Banke,Derek Bowie,Hey Kyoung Lee,Richard L. Huganir,Arne Schousboe,Stephen F. Traynelis +5 more
TL;DR: It is suggested that AMPA receptor peak response open probability can be increased by PKA through phosphorylation of GluR1 Ser845.
Journal ArticleDOI
Inward Rectification of Both AMPA and Kainate Subtype Glutamate Receptors Generated by Polyamine-Mediated Ion Channel Block
Derek Bowie,Mark L. Mayer +1 more
TL;DR: CA2+-permeable glutamate receptors assembled from subunits containing a GLN residue at the RNA editing site in membrane domain 2 show strong inward rectification, and analysis of the voltage dependence of whole-cell responses predicted intracellular free spermine and spermidine concentrations of 51 and 153 muM, respectively.
Journal ArticleDOI
Ionotropic glutamate receptors & CNS disorders.
TL;DR: It is argued that the understanding of iGluRs has reached a critical turning point to permit, for the first time, a comprehensive re-evaluation of their role in the cause of disease.
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Excitotoxic death of retinal neurons in vivo occurs via a non-cell-autonomous mechanism.
Frédéric Lebrun-Julien,L. Duplan,Vincent Pernet,Ingrid K. Osswald,Przemyslaw Sapieha,Philippe Bourgeois,Kathleen M. Dickson,Derek Bowie,Philip A. Barker,Adriana Di Polo +9 more
TL;DR: The data reveal a novel non-cell-autonomous mechanism by which glial cells can profoundly exacerbate neuronal death following excitotoxic injury, and this cell loss occurs mainly through a TNFα-dependent increase in Ca2+-permeable AMPA receptors on susceptible neurons.