The effect of drugs on accumulation of monoamines in tubero-infundibular dopamine neurons
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TL;DR
The present results indicate that the mechanism at the nerve cell membrane of the dopamine neurons in fundamentally different from that in the noradrenaline neurons, since it was not blocked by desipramine, chlorpromazine or guanethidine which block this mechanism in the NA neurons.
Abstract
Histochemical studies have been carried out on the effects drugs on the accumulation of monoamines in the tubero-infundibular dopamine neurons of rat after preceding depletion. It was found that (+)-amphetamine and cocaine blocked the reserpine-resistant accumulation of dopamine, noradrenaline and α-methyl-noradrenaline; desipramine, guanethidine and chlorpromazine did not block the accumulation of these amines. Very high doses of 5-hydroxytryptamine, given after depletion with reserpine caused an accumulation of 5-hydroxytryptamine which was blocked by (+)-amphetamine. The mechanism at the nerve cell membrane, which is able to take up and concentrate amines and which is resistant to reserpine in contrast to the reserpine-sensitive storage mechanism, was not stereospecific. The accumulation of catecholamines observed after their injection to reserpine pretreated rats could be released by (+)-amphetamine but not by cocaine. The present results indicate that the mechanism at the nerve cell membrane of the dopamine neurons in fundamentally different from that in the noradrenaline neurons, since it was not blocked by desipramine, chlorpromazine or guanethidine which block this mechanism in the NA neurons. Furthermore, cocaine may block this mechanism in the DA neurons.
