Abstract
Neuronal death induced by activating N-methyl-D-aspartate (NMDA) receptors has been linked to Ca2+ and Na+ influx through associated channels. Whole-cell recording from cultured mouse cortical neurons revealed a NMDA-evoked outward current, INMDA-K, carried by K+ efflux at membrane potentials positive to -86 millivolts. Cortical neurons exposed to NMDA in medium containing reduced Na+ and Ca2+ (as found in ischemic brain tissue) lost substantial intracellular K+ and underwent apoptosis. Both K+ loss and apoptosis were attenuated by increasing extracellular K+, even when voltage-gated Ca2+ channels were blocked. Thus NMDA receptor-mediated K+ efflux may contribute to neuronal apoptosis after brain ischemia.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Apoptosis*
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Calcium / metabolism
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Calcium / pharmacology
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Calcium Channels / metabolism
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Cells, Cultured
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Cerebral Cortex / cytology*
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Cerebral Cortex / metabolism
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Culture Techniques
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Glutamic Acid / metabolism
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Ion Channel Gating
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Ion Transport
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Membrane Potentials
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Mice
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N-Methylaspartate / pharmacology
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Neocortex / cytology
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Neocortex / embryology
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Neocortex / metabolism
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Neurons / cytology*
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Neurons / metabolism
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Patch-Clamp Techniques
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Potassium / metabolism*
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Receptors, N-Methyl-D-Aspartate / metabolism*
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Sodium / metabolism
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Sodium / pharmacology
Substances
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Calcium Channels
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Receptors, N-Methyl-D-Aspartate
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Glutamic Acid
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N-Methylaspartate
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Sodium
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Potassium
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Calcium