Abstract
AbstractThe effects of chronic administration of antidepressant drugs and 2-phenylethylamine on β-adrenoceptor function were assessed. Monoamine oxidase inhibitors [phenelzine sulfate, 5 or 10mg kg−1 per day, and (−)-deprenyl HCI, 1mg kg−1 per day] and 2-phenylethylamine HCI (10mg kg−1 per day) were administered to male Sprague-Dawley rats via Alzet osmotic minipumps. On days 21 and 22, the motor-suppressant actions of the β-adrenoceptor agonist salbutamol hemisulfate (3mg kg−1 intraperitoneally after 15 min) were assessed as a measure of β-adrenoceptor sensitivity. On day 28, the animals were killed, and their brains were used for the measurement of monoamine oxidase activity and concentrations of 2-phenylethylamine, an endogenous amine and a metabolite of phenelzine. Phenelzine sulfate at 10mg kg−1 per day (but not 5mg kg−1 per day) and the combination of (−)-deprenyl and 2-phenylethylamine resulted in a decrease in the response to salbutamol. These treatments also resulted in substantial increases in brain 2-phenylethylamine concentrations. The phenelzine treatments each resulted in an equivalent inhibition of brain monoamine oxidase activity. These results support the proposal that 2-phenylethylamine may, at least in part, mediate the effects of phenelzine on β-adrenoceptor function.
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