Abstract
The effect of hydroxyl radical scavengers on acetylcholine (ACh) release evoked by nitric oxide (NO) generators and N-methyl-D-aspartate (NMDA) was investigated. Dimethylthiourea enhanced dose-dependently NO generators-evoked ACh release. Similarly, uric acid and mannitol significantly facilitated ACh release evoked by NO generators. The NMDA-induced ACh release was also significantly facilitated by hydroxyl radical scavengers. These scavengers themselves showed no effects on ACh release. These results suggest that hydroxyl radicals may modify the mechanism for NO-evoked ACh release.
MeSH terms
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Acetylcholine / metabolism*
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Analysis of Variance
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Animals
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Cells, Cultured
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Cerebral Cortex / drug effects*
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Cerebral Cortex / metabolism
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Free Radical Scavengers / pharmacology*
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Hydroxyl Radical*
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Mannitol / pharmacology
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Mice
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Neurons / drug effects*
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Neurons / metabolism
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Nitric Oxide / physiology*
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Nitroprusside / pharmacology
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Penicillamine / analogs & derivatives
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Penicillamine / pharmacology
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S-Nitroso-N-Acetylpenicillamine
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Thiourea / analogs & derivatives
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Thiourea / pharmacology
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Uric Acid / pharmacology
Substances
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Free Radical Scavengers
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Nitroprusside
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Uric Acid
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Nitric Oxide
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Hydroxyl Radical
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Mannitol
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S-Nitroso-N-Acetylpenicillamine
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1,3-dimethylthiourea
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Penicillamine
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Thiourea
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Acetylcholine