IgG Isolated from LP-BM5 Infected Mouse Brain Activates Ionotropic Glutamate Receptors

Biochemical and immunological studies have shown that mice infected with LP-BM5 virus develop antibodies to ionotropic glutamate receptors. Here, IgG isolated from brain of infected mice has been tested electrophysiologically on cultured rat cortical and hippocampal neurons. The IgG elicited glycine...

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Main Authors: Anthony S. Basile, Elena Koustova, P. Ioan, S. Rizzoli, Michael A. Rogawski, Peter N.R. Usherwood
Format: Article
Language:English
Published: Elsevier 2001-12-01
Series:Neurobiology of Disease
Online Access:http://www.sciencedirect.com/science/article/pii/S0969996101904425
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spelling doaj-42616dc36a624019861339009b9581702021-03-20T04:47:21ZengElsevierNeurobiology of Disease1095-953X2001-12-018610691081IgG Isolated from LP-BM5 Infected Mouse Brain Activates Ionotropic Glutamate ReceptorsAnthony S. Basile0Elena Koustova1P. Ioan2S. Rizzoli3Michael A. Rogawski4Peter N.R. Usherwood5Laboratory of Bioorganic Chemistry, NIDDKD, National Institutes of Health, Bethesda, Maryland, 20892; Epilepsy Research Branch, NINDS, National Institutes of Health, Bethesda, Maryland, 20892; Division of Molecular Toxicology, School of Life and Environmental Sciences, University Park, University of Nottingham, Nottingham, NG7 2RD, United KingdomLaboratory of Bioorganic Chemistry, NIDDKD, National Institutes of Health, Bethesda, Maryland, 20892; Epilepsy Research Branch, NINDS, National Institutes of Health, Bethesda, Maryland, 20892; Division of Molecular Toxicology, School of Life and Environmental Sciences, University Park, University of Nottingham, Nottingham, NG7 2RD, United KingdomLaboratory of Bioorganic Chemistry, NIDDKD, National Institutes of Health, Bethesda, Maryland, 20892; Epilepsy Research Branch, NINDS, National Institutes of Health, Bethesda, Maryland, 20892; Division of Molecular Toxicology, School of Life and Environmental Sciences, University Park, University of Nottingham, Nottingham, NG7 2RD, United KingdomLaboratory of Bioorganic Chemistry, NIDDKD, National Institutes of Health, Bethesda, Maryland, 20892; Epilepsy Research Branch, NINDS, National Institutes of Health, Bethesda, Maryland, 20892; Division of Molecular Toxicology, School of Life and Environmental Sciences, University Park, University of Nottingham, Nottingham, NG7 2RD, United KingdomLaboratory of Bioorganic Chemistry, NIDDKD, National Institutes of Health, Bethesda, Maryland, 20892; Epilepsy Research Branch, NINDS, National Institutes of Health, Bethesda, Maryland, 20892; Division of Molecular Toxicology, School of Life and Environmental Sciences, University Park, University of Nottingham, Nottingham, NG7 2RD, United KingdomLaboratory of Bioorganic Chemistry, NIDDKD, National Institutes of Health, Bethesda, Maryland, 20892; Epilepsy Research Branch, NINDS, National Institutes of Health, Bethesda, Maryland, 20892; Division of Molecular Toxicology, School of Life and Environmental Sciences, University Park, University of Nottingham, Nottingham, NG7 2RD, United KingdomBiochemical and immunological studies have shown that mice infected with LP-BM5 virus develop antibodies to ionotropic glutamate receptors. Here, IgG isolated from brain of infected mice has been tested electrophysiologically on cultured rat cortical and hippocampal neurons. The IgG elicited glycine-independent currents that reversed at ∼0 mV. Equivalent concentrations of IgG from uninfected mice were inactive. The glycine-independent currents were less influenced by DNQX and GYKI-52466 than currents elicited by AMPA and KA. The IgG also elicited glycine-dependent currents that reversed at −10 mV and were blocked by dl-AP5, 5,7-DCKA, and polyamine amides. Glycine-dependent and -independent currents were unaffected by tetrodotoxin, strychnine, the transmembrane Cl− gradient or d-tubocurare. Although part of the glycine-independent current remains uncharacterized, these results confirm that a virus-induced immunopathology produces IgG clones that activate ionotropic glutamate receptors and that could, thereby, contribute to the excitotoxic neurological syndrome observed in LP-BM5-infected mice.http://www.sciencedirect.com/science/article/pii/S0969996101904425
collection DOAJ
language English
format Article
sources DOAJ
author Anthony S. Basile
Elena Koustova
P. Ioan
S. Rizzoli
Michael A. Rogawski
Peter N.R. Usherwood
spellingShingle Anthony S. Basile
Elena Koustova
P. Ioan
S. Rizzoli
Michael A. Rogawski
Peter N.R. Usherwood
IgG Isolated from LP-BM5 Infected Mouse Brain Activates Ionotropic Glutamate Receptors
Neurobiology of Disease
author_facet Anthony S. Basile
Elena Koustova
P. Ioan
S. Rizzoli
Michael A. Rogawski
Peter N.R. Usherwood
author_sort Anthony S. Basile
title IgG Isolated from LP-BM5 Infected Mouse Brain Activates Ionotropic Glutamate Receptors
title_short IgG Isolated from LP-BM5 Infected Mouse Brain Activates Ionotropic Glutamate Receptors
title_full IgG Isolated from LP-BM5 Infected Mouse Brain Activates Ionotropic Glutamate Receptors
title_fullStr IgG Isolated from LP-BM5 Infected Mouse Brain Activates Ionotropic Glutamate Receptors
title_full_unstemmed IgG Isolated from LP-BM5 Infected Mouse Brain Activates Ionotropic Glutamate Receptors
title_sort igg isolated from lp-bm5 infected mouse brain activates ionotropic glutamate receptors
publisher Elsevier
series Neurobiology of Disease
issn 1095-953X
publishDate 2001-12-01
description Biochemical and immunological studies have shown that mice infected with LP-BM5 virus develop antibodies to ionotropic glutamate receptors. Here, IgG isolated from brain of infected mice has been tested electrophysiologically on cultured rat cortical and hippocampal neurons. The IgG elicited glycine-independent currents that reversed at ∼0 mV. Equivalent concentrations of IgG from uninfected mice were inactive. The glycine-independent currents were less influenced by DNQX and GYKI-52466 than currents elicited by AMPA and KA. The IgG also elicited glycine-dependent currents that reversed at −10 mV and were blocked by dl-AP5, 5,7-DCKA, and polyamine amides. Glycine-dependent and -independent currents were unaffected by tetrodotoxin, strychnine, the transmembrane Cl− gradient or d-tubocurare. Although part of the glycine-independent current remains uncharacterized, these results confirm that a virus-induced immunopathology produces IgG clones that activate ionotropic glutamate receptors and that could, thereby, contribute to the excitotoxic neurological syndrome observed in LP-BM5-infected mice.
url http://www.sciencedirect.com/science/article/pii/S0969996101904425
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