Changes in catecholaminergic pathways innervating the rat heart ventricle during morphine dependence. Involvement Of alpha(1)- and alpha(2)-adrenoceptors

Abstract

In the present study, we examined the effects of alpha(1)- and the alpha(2)-adrenoceptors blockade on the changes in the ventricular content of catecholamines in rats withdrawn from morphine. Rats were given morphine by s.c. implantation of morphine pellets for 5 days. On the seventh day, morphine withdrawal was induced by s.c. administration of naloxone (1 mg/kg), and rats were killed 30 min later. Pretreatment with yohimbine (alpha(2)-adrenoceptor) or prazosin (alpha(1)-adrenoceptor) 15 min prior to naloxone administration attenuated some of the behavioural signs of morphine withdrawal. In addition, biochemical analysis indicated that yohimbine completely abolished the withdrawal-induced increase in noradrenaline and dopamine turnover in the right ventricle. By contrast, prazosin did not block the hyperactivity of catecholaminergic neurons in the heart during withdrawal. These data suggest that the hyperactivity of catecholaminergic neurons in the heart during morphine withdrawal is dependent upon alpha(2)-adrenoceptor activation. In addition, the present results rule out the involvement of alpha(1)-adrenoceptors.