Abstract
Delayed damage to hippocampal CA1 pyramidal cells was observed in rats subjected to cerebral ischemia caused by 10 min of 4-vessel occlusion. Animals pretreated with alpha-fluoromethylhistidine, a suicide inhibitor of histidine decarboxylase, showed significantly more necrotic cells than did control animals. Mepyramine (H1-antagonist) and (R) alpha-methylhistamine (H3-agonist), but not zolantidine (H2-antagonist), significantly aggravated the delayed neuronal death. These results suggest that histaminergic neurons have a protective role, probably via H1-receptors, in the development of delayed neuronal death caused by cerebral ischemia.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Benzothiazoles
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Brain Ischemia / chemically induced*
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Brain Ischemia / pathology
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Cell Death / drug effects
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Hippocampus / blood supply*
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Hippocampus / cytology
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Histamine Agonists / toxicity
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Histamine H1 Antagonists / toxicity
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Histamine H2 Antagonists / toxicity
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Male
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Methylhistamines / toxicity
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Methylhistidines / toxicity
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Neurons / drug effects*
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Phenoxypropanolamines
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Piperidines / toxicity
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Pyrilamine / toxicity
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Rats
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Rats, Wistar
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Receptors, Histamine / drug effects*
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Synaptic Transmission / drug effects*
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Thiazoles / toxicity
Substances
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Benzothiazoles
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Histamine Agonists
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Histamine H1 Antagonists
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Histamine H2 Antagonists
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Methylhistamines
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Methylhistidines
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Phenoxypropanolamines
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Piperidines
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Receptors, Histamine
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Thiazoles
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alpha-methylhistamine
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alpha-fluoromethylhistidine
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Pyrilamine
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zolantidine