Effects of morphine intoxication on brain catecholamine neurons
1969
Abstract An inhibitor of catecholamine biosynthesis (α-methyltyrosine methyl ester; H 44/68) was administered to rats in various phases of morphine intoxication and withdrawal. After biosynthesis had been abolished the degree of catecholamine depletion was used as an index of the impulse flow within the catecholamine neurons. The biochemical estimations were supplemented by fluorescence histochemistry. Acute administration of morphine was found to cause an accelerated depletion of brain dopamine after catecholamine synthesis inhibition, which was interpreted as an increased activity within the ascending dopamine neuron system compared with controls. During chronic administration of morphine this effect on brain dopamine disappeared and the impulse flow became normal within this neuron system. Abrupt withdrawal was connected with a reduced activity in the brain dopamine neurons. Nalorphine-induced abstinence caused increased activity within the noradrenaline neuron systems in practically all parts of the brain, possibly as an effect of stress.
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