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Central β-adrenoceptor regulation and adaptation under physiological and pathophysiological conditions

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IUPHAR 9th International Congress of Pharmacology London 1984

Abstract

Most clinically effective antidepressant treatments — pharmacotherapy and electroconvulsive therapy (ECT) — attenuate the norepinephrine (NE) [noradrenaline] sensitive adenylate cyclase system and this attenuation is generally linked to a down-regulation of its β-adrenoceptor subpopulation (Sulser, 1983). Since catecholamine receptor coupled adenylate cyclase systems function as highly efficient kinetic amplification systems, small changes in receptor number and function, such as the formation of the second messenger cyclic AMP, will be amplified through the cascade of protein kinase mediated phosphorylation processes. Utilizing the β-adrenoceptor-cyclic AMP mediated formation of melatonin in the pineal gland, Heydorn et al. (1982) have demonstrated that the net effect on NE signal transfer following chronic treatment with antidepressants — both tricyclics and MAO inhibitors — is a deamplification of the NE signal.

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William Paton James Mitchell Paul Turner Cheryl Padgham Eileen Ashcroft

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© 1984 Macmillan Publishers Limited

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Sulser, F., Gillespie, D.D., Manier, D.H. (1984). Central β-adrenoceptor regulation and adaptation under physiological and pathophysiological conditions. In: Paton, W., Mitchell, J., Turner, P., Padgham, C., Ashcroft, E. (eds) IUPHAR 9th International Congress of Pharmacology London 1984. Palgrave Macmillan, London. https://doi.org/10.1007/978-1-349-17615-1_19

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