Both Paton (1957) and Schaumann (1957) have shown that morphine inhibits the release of acetylcholine from the isolated guinea-pig ileum suspended in eserinized physiological salt solution. The resting output of acetylcholine as well as the output during stimulation of the nerve endings in the intestinal wall is reduced when morphine is present in the bath fluid. According to these authors the inhibition of acetylcholine release is responsible for the paralysing action of morphine on the guinea-pig intestine. The present experiments were designed to find out whether morphine similarly depresses the release of acetylcholine from the central nervous system.When the cerebral ventricles of the cat are perfused with physiological salt solution containing an anticholinesterase acetylcholine appears in the effluent and it has recently been shown (Beleslin, Carmichael & Feldberg, 1964) that the greatest amount originates from structures lining the anterior horns of the lateral ventricles. In the present experiments therefore the method of perfusing the anterior horn of a lateral ventricle with an anticholinesterase was used to study the effect of morphine on the output of acetylcholine. In a similar way, the effect of chloralose was examined. METHODSCats of both sexes weighing between 1-8 and 3-6 kg were anaesthetized with chloralose (40-70 mg/kg) injected into the cannulated right femoral vein. To allow cannulation of the femoral vein, anaesthesia was induced with ethyl chloride and ether. The trachea was cannulated. With the cat lying on its belly the head was fixed to the ear bars and the mouthpiece of a head holder similar to that of a Horsley-Clark stereotaxic instrument. The surface of the skull was widely exposed and the muscles covering the atlanto-occipital membrane were dissected away.The anterior horn of the left lateral ventricle was perfused with neostigmine methyl sulphate in a concentration of 1/50,000. The method used was that of multiple cannulation of the ventricular system which is based on the principle that drugs perfused through one part of the ventricular system are denied access to those parts which are cannulated and perfused with artificial c.s.f. t NATO Science Fellow.

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Blood samples were collected from anaesthetized cats during haemorrhage or stimulation of the peripheral end of the vagus. Vasopressin and oxytocin were estimated in the samples by assaying alcohol extracts for antidiuretic activity in the water loaded rat and for milk-ejecting activity in the lactating guinea-pig. Haemorrhage caused vasopressin to be released into the blood with out detectable amounts of oxytocin. A similar result was obtained with vagal stimulation provided that the fall of blood pressure which it produced exceeded a critical value of about 80 mmHg. Failure to detect oxytocin in blood samples containing vasopressin was not due to the presence of adrenaline or any other inhibitory substance in the extracts blocking the response of the mammary gland to oxytocin. The stimulus for the independent release of vasopressin by haemorrhage appears to be the associated fall in arterial blood pressure.

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