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Enhancement of the responsiveness of cortical adrenergic receptors by chronic administration of the 5-hydroxytryptamine uptake inhibitor citalopram.

Authors


Address correspondence and reprint requests to Dr. J. Vetulani at Institute of Pharmacology, Polish Academy of Sciences, Smetna 12, PL-31-343 Krak6w, Poland.

Abstract

Abstract: The aim of this study was to evaluate the effect of citalopram, a second generation antidepressant agent producing no β-down-regulation, on the receptors and second messenger systems related to noradrenergic transmission in the cerebral cortex of the rat. We confirmed that citalopram does not bind to α1-, α2-, and β2-adrenoceptors, but we found that it attenuates the inhibitory action of the protein kinase C activator, 12-O-tetradecanoylphorbol 13-acetate, on the noradrenergic response from α1-adrenoceptor. In contrast to most antidepressants, chronic treatment with citalopram does not produce β-down-regulation, but increases the responses to noradrenaline from β-adrenoceptors without increasing the β1,-adrenoceptor density. Chronic treatment with citalopram also increases the maximal response from α1-adrenoceptor. The results indicate that β-down-regulation is not a necessary characteristic of an efficient antidepressant drug.

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