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• W2156715212 startingPage "7727" @default.
• W2156715212 abstract "The widespread neuronal injury that results after brief activation of highly Ca 2+ -permeable NMDA channels may, in large part, reflect mitochondrial Ca 2+ overload and the consequent production of injurious oxygen radicals. In contrast, AMPA/kainate receptor activation generally causes slower toxicity, and most studies have not found evidence of comparable oxygen radical production. Subsets of central neurons, composed mainly of GABAergic inhibitory interneurons, express AMPA/kainate channels that are directly permeable to Ca 2+ ions. Microfluorometric techniques were performed by using the oxidation-sensitive dye hydroethidine (HEt) to determine whether the relatively rapid Ca 2+ flux through AMPA/kainate channels expressed on GABAergic neurons results in oxygen radical production comparable to that triggered by NMDA. Consistent with previous studies, NMDA exposures triggered increases in fluorescence in most cultured cortical neurons, whereas high K + (50 m m ) exposures (causing depolarization-induced Ca 2+ influx through voltage-sensitive Ca 2+ channels) caused little fluorescence change. In contrast, kainate exposure caused fluorescence increases in a distinct subpopulation of neurons; immunostaining for glutamate decarboxylase revealed the responding neurons to constitute mainly the GABAergic population. The effect of NMDA, kainate, and high K + exposures on oxygen radical production paralleled the effect of these exposures on intracellular Ca 2+ levels when they were monitored with the low-affinity Ca 2+ -sensitive dye fura-2FF, but not with the high-affinity dye fura-2. Inhibition of mitochondrial electron transport with CN − or rotenone almost completely blocked kainate-triggered oxygen radical production. Furthermore, antioxidants attenuated neuronal injury resulting from brief exposures of NMDA or kainate. Thus, as with NMDA receptor activation, rapid Ca 2+ influx through Ca 2+ -permeable AMPA/kainate channels also may result in mitochondrial Ca 2+ overload and consequent injurious oxygen radical production." @default.
• W2156715212 created "2016-06-24" @default.
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• W2156715212 creator A5043030783 @default.
• W2156715212 date "1998-10-01" @default.
• W2156715212 modified "2023-10-18" @default.
• W2156715212 title "Rapid Ca²⁺Entry through Ca²⁺-Permeable AMPA/Kainate Channels Triggers Marked Intracellular Ca²⁺Rises and Consequent Oxygen Radical Production" @default.
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• W2156715212 doi "https://doi.org/10.1523/jneurosci.18-19-07727.1998" @default.
• W2156715212 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6793031" @default.
• W2156715212 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/9742143" @default.
• W2156715212 hasPublicationYear "1998" @default.
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