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Title: Long-term effect of antidepressant drugs and electroconvulsive shock on brain alpha 1-adrenoceptors following destruction of noradrenergic or serotonergic nerve terminals. Author: Nowak G, Przegaliński E. Journal: Pol J Pharmacol Pharm; 1988; 40(4):393-400. PubMed ID: 2851781. Abstract: Antidepressant drugs and electroconvulsive shock (ECS) given repeatedly increase the density of brain alpha 1-adrenoceptors. However, the mechanism involved in this effect is unknown. To study the role of presynaptic noradrenaline (NA) and 5-hydroxytryptamine (5-HT) nerve terminals in the above phenomenon we examined the density of [3H]prazosin binding sites in the rat cerebral cortex following a prolonged treatment with imipramine and citalopram (10 mg/kg po, twice daily for 14 days) or ECS (once daily for 8 days) in animals pretreated with DSP-4 (62.5 mg/kg ip) and p-chloroamphetamine (PCA, 2 x 10 mg/kg ip). In normal rats imipramine, citalopram and ECS increased the density (Bmax) of [3H]prazosin binding sites by 30, 25 and 19%, respectively. DSP-4 pretreatment abolished the effect of imipramine and citalopram but not that of ECS. Pretreatment with PCA influenced the effect of neither antidepressant drugs nor ECS. Our results indicate that the "up-regulation" of alpha 1-adrenoceptors induced by imipramine and citalopram, but not by ECS, depends on intact NA nerve terminals. They also show that the 5-HT system is not involved in the above phenomenon.[Abstract] [Full Text] [Related] [New Search]