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Ian J. Reynolds
Researcher at United States Military Academy
Publications - 160
Citations - 15525
Ian J. Reynolds is an academic researcher from United States Military Academy. The author has contributed to research in topics: NMDA receptor & Glutamate receptor. The author has an hindex of 69, co-authored 160 publications receiving 14872 citations. Previous affiliations of Ian J. Reynolds include University of Hong Kong & Oregon Health & Science University.
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Glutamate induces the production of reactive oxygen species in cultured forebrain neurons following NMDA receptor activation
TL;DR: A critical role for mitochondria in the production of ROS in association with glutamate excitotoxicity is suggested, and the feasibility of measuring theProduction of ROS at the level of the single cell is demonstrated.
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Mitochondrial depolarization in glutamate-stimulated neurons : an early signal specific to excitotoxin exposure
R. James White,Ian J. Reynolds +1 more
TL;DR: In this article, the authors used indo-1 microfluorometry and a specific inhibitor of the mitochondrial Na+/Ca2+ exchanger, CGP-37157, to demonstrate that mitochondria accumulate large quantities of Ca2+ during a toxic glutamate stimulus and further that Ca2− efflux from mitochondria contributes to the prolonged [Ca 2+]i elevation after glutamate removal.
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Glutamate-induced neuron death requires mitochondrial calcium uptake.
TL;DR: Results indicate that very high levels of cytoplasmic calcium are not necessarily toxic to forebrain neurons, and that potential-driven uptake of calcium into mitochondria is required to trigger NMDA-receptor-stimulated neuronal death.
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DeltaPsi(m)-Dependent and -independent production of reactive oxygen species by rat brain mitochondria.
TL;DR: It is demonstrated that rat brain mitochondria can be effective producers of ROS, however, the optimal conditions for ROS generation require either a hyperpolarized membrane potential or a substantial level of complex’I inhibition.
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Persistent Activation of ERK Contributes to Glutamate-induced Oxidative Toxicity in a Neuronal Cell Line and Primary Cortical Neuron Cultures
Madalina Stanciu,Ying Wang,Ruth Kentor,Nancy V Burke,Simon C. Watkins,Geraldine J. Kress,Ian J. Reynolds,Eric Klann,Maria R. Angiolieri,Jon W. Johnson,Donald B. DeFranco +10 more
TL;DR: It is shown that delayed and persistent activation of ERKs is associated with glutamate-induced oxidative toxicity in HT22 cells and immature primary cortical neuron cultures, and that U0126, a specific inhibitor of the ERK-activating kinase, MEK-1/2, protects both HT22cells and immaturePrimary cortex neuron cultures from glutamate toxicity.