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1 Intraperitoneal and intragastric (i.g.) administration of prostaglandin precursors arachidonic (2 mg, 15 mg/kg, i.p.; 30 mg/kg, i.g.), linolenic (100 mg/kg, i.p.; 200 mg/kg, i.g.) and linoleic (15, 100 mg/kg, i.p.; 100 mg/kg, i.g.) acids to 22 h food‐deprived rats inhibits food intake. 2 This anorexia is similar to that induced by prostaglandin F2α (1 mg/kg, i.p.). 3 At anorectic doses these fatty acids do not cause pyrexia, in fact arachidonic acid causes hypothermia. 4 Prior treatment with indomethacin (15 mg/kg) and paracetamol (50 mg/kg) specifically reverses the anorexia and the behavioural satiety induced by the three fatty acids, while not affecting prostaglandin F2α‐induced suppression of food intake. 5 Results of the present experiments suggest that both physiological and pharmacological modification of appetite could be brought about through an effect on prostaglandin generating systems.

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I Intracerebroventricular injection of prostanglandin F2a (10-40 jg) decreases food intake in a dosedependent manner in rats trained to consume their daily total food intake in a 2 h period. 2 This anorexia is also observed in satiated rats, which had ad libitum access to food. 3 The anorectic activity of prostaglandin F2a is not modified by changes in the internal environment of the body after food intake, such as increased blood glucose and insulin levels and decreased fatty acid levels, or by the presence or absence of food in the stomach, as is evident from the anorectic activity of prostaglandin F2a in partially satiated rats. 4 The anorexia is not due to pain or irritative properties of prostaglandin F2a since induction of comparable pain with 3% acetic acid does not affect food intake in rats deprived of food for 22 hours. 5 Anorectic doses of prostaglandin F2a when injected intraperitoneally cause hypothermia.6 The results suggest that the inhibitory activity of prostaglandin F2a on food intake is at both peripheral and central sites. 7 Prostaglandin F2a-induced anorexia is associated with the behavioural tranquillization that is seen after the ingestion of food.

Summary1. Ouabain given by intracerebroventricular injection to mice in small doses (0-1-04 jg) produced a dose related depression of central nervous activity, characterized by a reduction in spontaneous locomotor activity, hypothermia, catalepsy and ptosis, lowered body posture and lack of response to external stimuli. Doses above 0 4 ,ug were excitatory, convulsant and lethal. 2. The depressant effects could be antagonized by (+)-amphetamine, desmethylimipramine, dibutyryl cyclic 3'5'-adenosine monophosphate and caffeine. 3. The MAO inhibitor nialamide produced only a small antagonism of ouabain, resulting in a greater rate of recovery from the depressant effects of ouabain. 4. The depressant effects were associated with a marked elevation of wholebrain dopamine levels with little change in noradrenaline or 5-hydroxytryptamine.5. The dopamine-3-hydroxylase inhibitor sodium diethyldithiocarbamate, administered by intracerebroventricular injection, produced effects qualitatively similar to those seen after ouabain.6. An interference with central transmitter function is postulated as a possible r.'ode of action of intracerebroventricularly injected ouabain.