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To clarify whether monoamine neuron activity in the brain is regulated by histamine H3 receptors, the effects of a potent and selective H3 agonist, (R) alpha-methylhistamine and an antagonist, thioperamide, on monoamine metabolism were examined in the telencephalon, hypothalamus and brainstem of the rat and the whole mouse brain. Histamine turnover estimated from the pargyline-induced tele-methylhistamine accumulation decreased markedly with (R) alpha-methylhistamine administration (6.3 mg/kg i.p.) and increased with thioperamide administration (5 mg/kg i.p.) in all the brain regions examined. (R) alpha-Methylhistamine and thioperamide, at the doses tested, neither induced any significant changes in the levels of noradrenaline or 3,4-dihydroxyphenylacetic acid nor had any significant influence on the alpha-methyl-p-tyrosine-induced declines of the noradrenaline and dopamine levels in all the brain regions examined. However, thioperamide significantly decreased the dopamine level only in the rat telencephalon. In general, thioperamide increased 5-hydroxyindoleacetic acid (5-HIAA)/5-hydroxytryptamine (5-HT) ratios and pargyline-induced 5-HT accumulation. However, (R) alpha-methylhistamine affected neither the 5-HT nor the 5-HIAA level. The pargyline-induced 5-HT accumulation was slightly enhanced by (R) alpha-methylhistamine in the whole mouse brain. The enhancement by thioperamide of pargyline-induced 5-HT accumulation was not inhibited by (R) alpha-methylhistamine. These results suggest that H3 receptors have no important roles in the regulation of monoaminergic activity in contrast with their regulatory function in histaminergic activity. In addition, thioperamide at high doses may enhance 5-HT turnover independently of H3 receptors.
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