The Experts below are selected from a list of 11019 Experts worldwide ranked by ideXlab platform
Maurlee Scanlon - One of the best experts on this subject based on the ideXlab platform.
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The glutamate inhibition of carbachol stimulated inositol phosphate production in rat cortical cells is mediated through an Ionotropic NMDA Receptor
Neuroscience Letters, 1994Co-Authors: J. Ham, Maurlee ScanlonAbstract:Carbachol (0.1 mM) stimulated accumulation of inositol monophosphate (IP1) (3–4 fold of basal, P < 0.001) in fetal rat cortical cells is attenuated by glutamate (at 0.1 mM, 40–70% of carbachol alone, P < 0.001). This inhibition by glutamate was reduced by 2-amino-5-phosphonopentanoic acid (AP5), but not by γ-d-SCPnic acid (GAMS) or 2-amino-3-phosphonopropionic acid (AP3). The metabotropic Receptor agonist (1S,3R)-1-aminocyclopentane-1-3-dicarboxylic acid [(1S,3R)-ACPD] (up to 0.1 mM) had no effect upon carbachol stimulated IP1. Staurosporine and quinacrine were unable to prevent the inhibition of carbachol stimulated IP1 by glutamate. These data suggest that the inhibition of carbachol-stimulated IP1, by glutamate in rat cortical cells is mediated through an NMDA Ionotropic Receptor.
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The glutamate inhibition of carbachol stimulated inositol phosphate production in rat cortical cells is mediated through an Ionotropic NMDA Receptor.
Neuroscience letters, 1994Co-Authors: J. Ham, Maurlee ScanlonAbstract:Carbachol (0.1 mM) stimulated accumulation of inositol monophosphate (IP1) (3-4 fold of basal, P < 0.001) in fetal rat cortical cells is attenuated by glutamate (at 0.1 mM, 40-70% of carbachol alone, P < 0.001). This inhibition by glutamate was reduced by 2-amino-5-phosphonopentanoic acid (AP5), but not by gamma-D-glutamylaminomethyl sulphonic acid (GAMS) [corrected] or 2-amino-3-phosphonopropionic acid (AP3). The metabotropic Receptor agonist (1S,3R)-1-aminocyclopentane-1-3-dicarboxylic acid [(1S,3R)-ACPD] (up to 0.1 mM) had no effect upon carbachol stimulated IP1. Staurosporine and quinacrine were unable to prevent the inhibition of carbachol stimulated IP1 by glutamate. These data suggest that the inhibition of carbachol-stimulated IP1, by glutamate in rat cortical cells is mediated through an NMDA Ionotropic Receptor.
Leonard Maler - One of the best experts on this subject based on the ideXlab platform.
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balanced Ionotropic Receptor dynamics support signal estimation via voltage dependent membrane noise
Journal of Neurophysiology, 2016Co-Authors: Curtis M Marcoux, Stephen E Clarke, William H Nesse, Andre Longtin, Leonard MalerAbstract:Encoding behaviorally relevant stimuli in a noisy background is critical for animals to survive in their natural environment. We identify core biophysical and synaptic mechanisms that permit the en...
Stephen D Roper - One of the best experts on this subject based on the ideXlab platform.
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molecular and physiological evidence for glutamate umami taste transduction via a g protein coupled Receptora
Annals of the New York Academy of Sciences, 1998Co-Authors: Nirupa Chaudhari, Stephen D RoperAbstract:ABSTRACT: Recent molecular analyses have demonstrated that a metabotropic glutamate Receptor, mGluR4, is expressed in taste buds from rat circumvallate and foliate papillae. Behavioral studies demonstrated that l(+)-2-amino-4-phosphonobutyric acid (L-AP4), an agonist for mGluR4 and related Receptors, mimics the taste of monosodium glutamate (MSG) in rats. mGluR4 is known to signal through inhibition of the cyclic adenosine-5′,3′-monophosphate (cAMP) cascade. Circumvallate and foliate taste buds exhibit decreases of cAMP levels following stimulation with MSG, and the response is potentiated by 5′-inosine monophosphate, suggesting that it is related to umami taste. Further, experiments on mice with the mGluR4 gene knocked out support the interpretation that mGluR4 is a key component in glutamate taste. Glutamate may also stimulate taste buds through an Ionotropic Receptor pathway. In patch-clamp studies, glutamate evokes two types of currents, similar to those elicited by N-methyl-d-aspartate (N MDA) and L-AP4. We speculate upon the significance of two glutamate Receptor pathways in taste buds.
Michel Baudry - One of the best experts on this subject based on the ideXlab platform.
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Synaptic Efficacy as a Function of Ionotropic Receptor Distribution: A Computational Study.
PloS one, 2015Co-Authors: Sushmita L. Allam, Jean-marie C. Bouteiller, Nicolas Ambert, Renaud Greget, Serge Bischoff, Michel Baudry, Theodore W. BergerAbstract:Glutamatergic synapses are the most prevalent functional elements of information processing in the brain. Changes in pre-synaptic activity and in the function of various post-synaptic elements contribute to generate a large variety of synaptic responses. Previous studies have explored postsynaptic factors responsible for regulating synaptic strength variations, but have given far less importance to synaptic geometry, and more specifically to the subcellular distribution of Ionotropic Receptors. We analyzed the functional effects resulting from changing the subsynaptic localization of Ionotropic Receptors by using a hippocampal synaptic computational framework. The present study was performed using the EONS (Elementary Objects of the Nervous System) synaptic modeling platform, which was specifically developed to explore the roles of subsynaptic elements as well as their interactions, and that of synaptic geometry. More specifically, we determined the effects of changing the localization of Ionotropic Receptors relative to the presynaptic glutamate release site, on synaptic efficacy and its variations following single pulse and paired-pulse stimulation protocols. The results indicate that changes in synaptic geometry do have consequences on synaptic efficacy and its dynamics.
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EMBC - Influence of Ionotropic Receptor location on their dynamics at glutamatergic synapses
Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and Biology Society. Annual Inte, 2012Co-Authors: Sushmita L. Allam, Jean-marie C. Bouteiller, Nicolas Ambert, Renaud Greget, Serge Bischoff, Michel Baudry, Theodore W. BergerAbstract:In this paper we study the effects of the location of Ionotropic Receptors, especially AMPA and NMDA Receptors, on their function at excitatory glutamatergic synapses. As few computational models only allow to evaluate the influence of Receptor location on state transition and Receptor dynamics, we present an elaborate computational model of a glutamatergic synapse that takes into account detailed parametric models of Ionotropic Receptors along with glutamate diffusion within the synaptic cleft. Our simulation results underscore the importance of the wide spread distribution of AMPA Receptors which is required to avoid massive desensitization of these Receptors following a single glutamate release event while NMDA Receptor location is potentially optimal relative to the glutamate release site thus, emphasizing the contribution of location dependent effects of the two major Ionotropic Receptors to synaptic efficacy.
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Posttranslational regulation of Ionotropic glutamate Receptors and synaptic plasticity.
International review of neurobiology, 1998Co-Authors: Steve Standley, Michel BaudryAbstract:Publisher Summary This chapter summarizes the molecular properties and the subcellular localization of the two classes of glutamate Ionotropic Receptors, the AMPA (2-amino-3-(3-hydroxy-5-methyl-isoxazol-4-yl) propanoic acid) and N-methyl-D-aspartate (NMDA) Receptors. The results of studies concerning the phosphorylation of both AMPA and NMDA Receptors are reviewed. This is followed by a summary of the work on the characterization of calpain-mediated truncation of glutamate Ionotropic Receptor subunits and the roles of the phospholipid environment in the characteristics of the AMPA Receptors. Then information related to the targeting and anchoring of glutamate Receptors are reviewed before summarizing available data on the turnover of these Receptors. The chapter also discusses the possible functions of posttranslational modifications of glutamate Receptors in various physiological as well as pathological forms of synaptic plasticity. The posttranslational modifications of glutamate Ionotropic Receptors are well-suited to participate in the phenomena of long-term potentiation and long-term depression and that similar mechanisms might be responsible for changes in synaptic excitability observed following seizure activity or various forms of brain injury.
J. Ham - One of the best experts on this subject based on the ideXlab platform.
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The glutamate inhibition of carbachol stimulated inositol phosphate production in rat cortical cells is mediated through an Ionotropic NMDA Receptor
Neuroscience Letters, 1994Co-Authors: J. Ham, Maurlee ScanlonAbstract:Carbachol (0.1 mM) stimulated accumulation of inositol monophosphate (IP1) (3–4 fold of basal, P < 0.001) in fetal rat cortical cells is attenuated by glutamate (at 0.1 mM, 40–70% of carbachol alone, P < 0.001). This inhibition by glutamate was reduced by 2-amino-5-phosphonopentanoic acid (AP5), but not by γ-d-SCPnic acid (GAMS) or 2-amino-3-phosphonopropionic acid (AP3). The metabotropic Receptor agonist (1S,3R)-1-aminocyclopentane-1-3-dicarboxylic acid [(1S,3R)-ACPD] (up to 0.1 mM) had no effect upon carbachol stimulated IP1. Staurosporine and quinacrine were unable to prevent the inhibition of carbachol stimulated IP1 by glutamate. These data suggest that the inhibition of carbachol-stimulated IP1, by glutamate in rat cortical cells is mediated through an NMDA Ionotropic Receptor.
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The glutamate inhibition of carbachol stimulated inositol phosphate production in rat cortical cells is mediated through an Ionotropic NMDA Receptor.
Neuroscience letters, 1994Co-Authors: J. Ham, Maurlee ScanlonAbstract:Carbachol (0.1 mM) stimulated accumulation of inositol monophosphate (IP1) (3-4 fold of basal, P < 0.001) in fetal rat cortical cells is attenuated by glutamate (at 0.1 mM, 40-70% of carbachol alone, P < 0.001). This inhibition by glutamate was reduced by 2-amino-5-phosphonopentanoic acid (AP5), but not by gamma-D-glutamylaminomethyl sulphonic acid (GAMS) [corrected] or 2-amino-3-phosphonopropionic acid (AP3). The metabotropic Receptor agonist (1S,3R)-1-aminocyclopentane-1-3-dicarboxylic acid [(1S,3R)-ACPD] (up to 0.1 mM) had no effect upon carbachol stimulated IP1. Staurosporine and quinacrine were unable to prevent the inhibition of carbachol stimulated IP1 by glutamate. These data suggest that the inhibition of carbachol-stimulated IP1, by glutamate in rat cortical cells is mediated through an NMDA Ionotropic Receptor.
