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1. In unanaesthetized rabbits and cats reserpine was injected through a chronically implanted cannula in the left lateral cerebral ventricle, and rectal temperature was recorded.

2. In rabbits the reserpine (0·5-0·6 mg) caused a rise in temperature, frequent defaecation and sedation. On repeating the intraventricular injections at 24 hr intervals the rise in temperature was not obtained with the second or third injection, but defaecation and sedation still occurred. When the hyperthermic response to intraventricular reserpine had disappeared the anterior hypothalamus still responded to intraventricular noradrenaline which produced a rise in temperature.

3. In cats the reserpine (0·5-0·75 mg) caused a biphasic change in temperature, i.e. an initial fall followed by a rise, frequent defaecation, and catalepsy. On repeating the intraventricular injections at 24 hr intervals the initial hypothermic phase of the temperature response was not obtained with the second or third injection, but the late rise, defaecation and catalepsy were still produced. When the hypothermic phase had disappeared the hypothalamus still responded to intraventricular noradrenaline or adrenaline which produced a fall, and to intraventricular 5-hydroxytryptamine (5-HT) which produced a rise in temperature.

4. It is concluded that the rise in temperature in rabbits and the initial fall produced in cats is not due to a direct action of reserpine on the cells of the anterior hypothalamus but to noradrenaline released from adrenergic fibres ending at these cells. When these fibres are depleted of their noradrenaline by one or two injections of reserpine, these effects are not obtained because noradrenaline is no longer available to be released in sufficient amounts to raise temperature in rabbits and to lower it in cats.