Abstract
We have investigated in the present study the effect of Mg(2+)-valproate on necrotic degeneration induced by an excitotoxic insult in primary culture of cerebellar neurons, that is an homogeneous population of glutamatergic neurons. Mg(2+)-valproate protected cultures against glutamate-induced neurotoxicity, acting as an indirect N-methyl-D-aspartate (NMDA) receptor antagonist, thus reducing free radical formation and affecting the biochemical parameters (i.e. 45Ca(2+)-influx, cyclic GMP formation, inositol phospholipid hydrolysis and protein kinase C translocation) that undergo modifications following NMDA receptor activation in cerebellar granule cells.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Calcium / metabolism
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Cells, Cultured
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Cerebellum / chemistry
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Cerebellum / drug effects*
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Cyclic GMP / analysis
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Cyclic GMP / biosynthesis
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Free Radicals / analysis
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Glutamic Acid / metabolism
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Glutamic Acid / pharmacology
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Glutamic Acid / toxicity
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Magnesium / analysis
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Magnesium / pharmacology*
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Nerve Degeneration / drug effects*
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Neurons / chemistry*
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Neurons / drug effects*
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Neurotoxins / biosynthesis
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Rats
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Receptors, N-Methyl-D-Aspartate / drug effects
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Transfer RNA Aminoacylation / drug effects
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Valproic Acid / analysis
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Valproic Acid / pharmacology*
Substances
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Free Radicals
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Neurotoxins
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Receptors, N-Methyl-D-Aspartate
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Glutamic Acid
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Valproic Acid
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Cyclic GMP
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Magnesium
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Calcium