—The injection of 50 μg of 5,6‐dihydroxytryptamine (5,6‐HT) into a lateral ventricle of the rat depleted the spinal cord and various regions of the brain of indoleamines (presumably 5‐HT) and 5‐hydroxyindole acetic acid. The concentrations of 5‐HT were measured by two different methods: the formation of a fluorescent derivative with o‐phthalaldehyde, and the native fluorescence in hydrochloric acid. When the results of both methods were compared on the pons and medulla 4 days after injecting 5,6‐HT, the loss in indoleamine appeared to be greater when o‐phthalaldehyde was used. This suggests that the two methods may be measuring different compounds. According to both methods, the loss of 5‐HT persisted for several days after the injection of 5,6‐HT, but by 2 months 5‐HT concentrations (measured only by the native fluorescence procedure), had recovered to near‐normal values. The depletion of 5‐HT was most pronounced in regions adjacent to the ventricular system and in the spinal cord. Initially, caudate and septum were more affected on the side of the injection, and later showed some permanent atrophy. The injection of up to 50 μg of 5,6‐HT did not lead to any significant loss of noradrenaline or dopamine from the brain, or to any reduction in the activity of the enzyme tyrosine hydroxylase. The drug was a potent inhibitor of the uptake of [3H]5‐HT by brain slices, but was less effective in inhibiting catecholamine uptake systems. These observations suggest a preferential action on tryptaminergic neurones. Larger doses of 5,6‐HT caused a loss of catecholamines and tyrosine hydroxylase from the brain, and were severely toxic.

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SUMMARY1. Although it is well established that exogenous noradrenaline injected into the diencephalon causes the satiated rat to eat, it is not known whether eating may be induced by release of endogenous diencephalic noradrenaline. In the present experiment 6-hydroxydopamine was injected into the diencephalon of the rat to release catecholamines and produce degeneration of catecholamine-containing neurones.2. Injection into the preoptic area of 001-16O ,0sg of 6-hydroxydopamine caused satiated rats to eat.3. All doses of 6-hydroxydopamine above 0.01 lug produced long-lasting partial depletion of noradrenaline and dopamine in the region of the brain composed of septum, preoptic area and hypothalamus. 4. Repeated injections of 8 ,ug 6-hydroxydopamine at intervals of several days caused progressively less eating.5. Eating in response to 6-hydroxydopamine was inhibited by pretreatment with desmethylimipramine, or by pre-treatment with the adrenergic blocking agents phentolamine or MJ-1999. 6. Water intake after 6-hydroxydopamine was reduced by pre-treatment with desmethylimipramine or MJ-1999 but was enhanced after pretreatment with phentolamine.7. It is concluded that release of diencephalic catecholamines by injection of 6-hydroxydopamine causes eating in rats and that the catecholamine responsible for eliciting eating is noradrenaline.