The turnover and metabolism of catecholamines after i.p. administration of 10 (low dose) or 40 (high dose) mg/kg of morphine sulfate were measured in the brain, lumbar spinal cord, heart, celiac and superior cervical ganglia (SCG) of demedullated rats with unilaterally decentralized SCG. Demedullation significantly increased norepinephrine concentration and turnover in both sham operated and decentralized SCG, but demedullation failed to change the turnover of dopamine (DA) in both ganglia. Low doses of morphine only increased DA metabolism in the caudate nucleus. High doses of morphine failed to change the turnover of norepinephrine stored in heart and sympathetic ganglia but produced variable changes in norepinephrine turnover in the spinal cord and brain. High doses of morphine significantly increased DA turnover and metabolism in the celiac ganglion, SCG, caudate nucleus and the spinal cord of demedullated rats. These effects of morphine were antagonized by naloxone. DA metabolism in decentralized SCG of demedullated and SCG of intact rats remained unchanged after high doses of morphine. The action of morphine on DA metabolism was facilitated by demedullation, suggesting that the adrenal medulla secretes a modulator that can counteract the effects of opiate ligands on ganglionic small intensely fluorescent cells. Atropine and hexamethonium failed to antagonize the increase in the metabolism of ganglionic DA produced by morphine; and the increase in ganglionic DA metabolism caused by oxotremorine was not antagonized by naloxone, thus confirming a disassociation between the action on ganglionic DA mediated by cholinergic and opiate receptors. Since decentralization of the SCG abolishes the increase in DA metabolism induced by morphine, stimulation of extraganglionic opiate receptors reflects the metabolism of DA located in small intensely fluorescent cells.