Abstract
The role of brain histamine on seizure development of pentylenetetrazol (PTZ)-induced kindling was examined in H(1)-receptor gene knockout (H(1)KO), histidine decarboxylase-deficient (HDC(-/-)) and mast cell-deficient (W/W(v)) mice. All H(1)KO, HDC(-/-) and W/W(v) mice had accelerated seizure development of PTZ-induced kindling when compared to their respective wild-type mice. The daily PTZ-kindling increased histamine content in the cortex and diencephalon of H(1)KO mice, whereas the histamine content in the diencephalon of W/W(v) mice was decreased. The present study indicates that histamine plays a suppressive role in seizure development through H(1)-receptors.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Analysis of Variance
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Animals
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Brain / drug effects
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Brain / metabolism
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Brain Chemistry
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Convulsants / administration & dosage
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Convulsants / adverse effects*
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Histamine / analysis
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Histidine Decarboxylase / deficiency
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Histidine Decarboxylase / genetics
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Histidine Decarboxylase / metabolism*
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Mast Cells / physiology*
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Mice
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Mice, Inbred Strains
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Mice, Knockout
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Pentylenetetrazole / administration & dosage
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Pentylenetetrazole / adverse effects*
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Receptors, Histamine H1 / deficiency
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Receptors, Histamine H1 / genetics
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Receptors, Histamine H1 / metabolism*
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Seizures / chemically induced*
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Seizures / genetics
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Seizures / metabolism
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Statistics, Nonparametric
Substances
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Convulsants
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Receptors, Histamine H1
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Histamine
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Histidine Decarboxylase
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Pentylenetetrazole