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1. Prostaglandins E1 (PGE1) was injected into the preoptic/anterior hypothalamic (PO/AH) area of the squirrel monkey. 2. Increases in rectal temperature (Tre) produced by PGE1 injections of 20 ng to 500 ng were dose‐dependent. 3. When ambient temperature (Ta) was below the thermoneutral zone, increases in Tre were produced entirely by increases in metabolic rate. With Ta at the upper end of the thermoneutral zone, increases in Tre were produced by vasoconstriction in addition to lesser increases in metabolic rate. 4. During sessions of behavioural temperature regulation, PGE1 injections were followed by the selection of a higher Ta, increased skin temperature and subsequent increases in Tre. 5. PGE1 injections produce dose‐dependent increases in Tre which are similar regardless of ambient temperature or whether behavioural or autonomic means are utilized to raise the heat content of the body.

1. Respiratory evaporative heat loss in the rabbit has a minimum value of 0‐2‐0‐3 W/kg and a maximum value of about 1‐1 W/kg in non‐evaporatively limited environments. 2. Both skin temperature and hypothalamic temperature influence respiratory evaporative heat loss, and they do so in a multiplicative fashion. Thus, at low skin temperature the hypothalamic temperature threshold for the onset of panting is above normal hypothalamic temperature and hypothalamic thermosensitivity is high. On the other hand, at high skin temperatures, the hypothalamic temperature threshold for the onset of panting is well below normal hypothalamic temperature, but hypothalamic thermosensitivity is greatly reduced. 3. The influence of mean skin temperature (Tsk) and hypothalamic temperature on respiratory evaporative heat loss (Eres) in the rabbit can be described by the equation: Eres=1‐1‐0‐08 (Tsk‐39‐7) (Thy‐42‐9) greater than or equal to 0‐3 W/kg. 4. Thus, the ability of a lowered mean skin temperature to increase the thermosensitivity of the hypothalamus in response to local temperature changes applies to heat loss mechanisms as well as heat production mechanisms. It is suggested that the characteristics of this peripheral input into the C.N.S. are fulfilled by tonic cold fibre input originating from the peripheral cold receptors on the body surface.

In rats, we tested the hypothesis that capsaicin desensitization reduces hypothalamic warm thermosensitivity. We locally heated and cooled the hypothalamus using water‐perfused thermodes while observing thermoregulatory variables. In untreated rats, a small dose of capsaicin had profound effects on thermoregulation. However, desensitizing rats to capsaicin had no effect on hypothalamic thermosensitivity for metabolic rate or changes in body temperature due to displacements of hypothalamic temperature. Contrary to current opinion, we conclude that capsaicin desensitization does not alter hypothalamic thermosensitivity to warm or cold.

Control febrile responses to intravenous injections of endogenous pyrogen were determined in groups of rabbits and rats, exposed to their respective thermoneutral ambient temperatures. Discrete electrolytic lesions were placed within the confines of the organum vasculosum laminae terminalis (o.v.l.t.) of each species. The fever responses of the animals were remeasured 3 days later, and in every case there was a marked enhancement of the fevers produced, using the same doses of endogenous pyrogen that were used earlier. Similar lesions that were placed unilaterally within the preoptic anterior hypothalamic area in groups of control animals, were not effective in enhancing the febrile responses of these animals. The course of this lesion‐induced fever enhancement in rabbits was studied during the succeeding 3 week period, when it was found to return gradually towards the control levels. It is postulated that the o.v.l.t. is involved in some manner in the process whereby circulating pyrogen is translated into a febrile stimulus. Lesions posited within this region are thought to either increase the amount of pyrogen entering the o.v.l.t., or to increase the sensitivity of pyrogen receptor sites within the o.v.l.t.

1. A method was devised to sample cerebrospinal fluid (c.s.f.) from the third ventricle of conscious rabbits.

1. Micro‐injections of prostaglandin E1(PGE1) into the anterior hypothalamus of the rabbit produced fever which was nearly immediate in onset. The prostaglandin sensitive region appears to be identical to that described as being fever sensitive to leucocytic pyrogen.