Behavioral thermoregulatory responses to hypothalamic cooling and warming in baboons☆

SUMMARY1. The cerebral ventricles of the unanaesthetized monkey were perfused at a rate of 50-100 4td./min with artificial cerebrospinal fluid (c.s.f.) containing 11F0-340 mm excess sodium or 23-9-47-9 mm excess calcium ions. By repeated perfusions, a marked hyperthermia elicited by excess sodium or deep hypothermia by excess calcium was sustained for up to half a day.2. During the sodium-induced hyperthermia or calcium-induced hypothermia, the monkey thermoregulated adequately around the new level of temperature in response to either 50 or 150 ml. water heated to 580 C or chilled to 00 C and given by the intragastric route. Cold water produced a transient hypothermia after which temperature returned to the pre-load level; hot water given in the same way evoked a short-lasting hyperthermia, and again the temperature returned just to the new setpoint level.3. Perfusions at 50 #1./min of isolated areas of the diencephalon by means of push-pull cannulae with a solution containing 110-34-0 mm excess sodium ions or 11L3-47-9 mm excess calcium ions altered the body temperature of the monkey only when the sites of perfusion were located in the mammillary region of the posterior hypothalamus. Following the prolonged hyperthermia produced by excess sodium ions or the deep hypothermia evoked by excess calcium ions in the push-pull perfusion fluid, the monkey thermoregulated around the new temperature level again in response to 150 ml. of either hot or cold water given in the stomach. R. D. MYERS AND T. L. YAKSH perature. When EGTA was perfused directly in the posterior hypothalamus by means of push-pull cannulae, a profound hyper-pyrexia ensued which could be abolished immediately by perfusing a solution of excess calcium at the same diencephalic site.5. During the calcium-induced hypothermia, the heart rate declined but the electrical activity of the cortex was relatively unchanged. Feeding was also elicited in the hypothermic monkey by noradrenaline microinjected at a site in the hypothalamus at which eating was evoked when the body temperature was normal.6. The evidence supports the hypothesis that in the primate, the inborn mechanism which establishes the set-point for body temperature at 370 C is the constancy in the intrinsic ratio between sodium and calcium ions within the posterior hypothalamus. If the set-point is elevated or lowered by a disturbance of the balance between these two cations, the monkey nevertheless can thermoregulate normally around the new level of body temperature.

Section: Discussionmentioning

confidence: 99%

Thermoregulation around a new ‘set‐point’ established in the monkey by altering the ratio of sodium to calcium ions within the hypothalamus

Myers¹,

Yaksh²

1971

“…Administration of bacterial and leucocyte pyrogens in cats (Weiss, Laties & Weiss, 1967), baboons (Gale, Mathews & Young, 1970), and dogs (Cabanac, Duclaux & Gillet, 1970) produces an increased demand for external heat. Wailer & Myers (1973) have shown that rhesus monkeys activate heat lamps more frequently following intrahypothalamic PGE, injections.…”

Section: Discussionmentioning

confidence: 99%

Behavioural and autonomic induction of prostaglandin E‐1 fever in squirrel monkeys.

Crawshaw¹,

Stitt²

1975

SUMMARY1. Prostaglandin 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 T1e.5. PGE1 injections produce dose-dependent increases in Te which are similar regardless of ambient temperature or whether behavioural or autonomic means are utilized to raise the heat content of the body.

“…In a similar setup at a thermoneutral environmental temperature, baboons increased their rate of lever pressing for heat reinforcement during the phase of rising temperature after Piromen injection. The rate ofresponding returned nearlyto pre-injection levels once bodytemperature had reached a plateau (Gale et al 1970). In another study when dogs, trained to control external sources of heat and cold, were given various pyrogens they responded more for heat than control animals at environmental temperatures below thermoneutrality and for less cold air at environmental temperatures above thermoneutrality (Cabanac et al 1970).…”

Section: Discussionmentioning

confidence: 94%

“…Elevation of the set-point for physiological thermoregulatory responses by pyrogens is accompanied by behavioural responses which facilitate the development of fever (Weiss, Laties & Weiss, 1967; Gale, Mathews & Young, 1970;Cabanac, Duclaux & Gillet, 1970). However, no studies have been reported in which thermoregulatory behaviour has been examined after administration of an agent which lowers the physiological set-point.…”

Section: Introductionmentioning

confidence: 99%

Complementary lowering of the behavioural and physiological thermoregulatory set‐points by tetrodotoxin and saxitoxin in the cat

Clark¹

1974

SUMMARY1. Injections oftetrodotoxin or saxitoxin (25 ng in 0 10 ml.) into a lateral cerebral ventricle caused deep body temperature of cats to fall approximately the same amount (20 C) whether the animals were resting in the cold (40 C) or were responding to escape heat.2. Continuous exposure to heat either prevented the hypothermic response or enhanced the level of tachypnoea required to lower body temperature. Tetrodotoxin also caused hypothermia when an animal was lever pressing to obtain heat in the cold environment.3. These results provide evidence that agents which alter the set-point for physiological thermoregulatory activity produce a complementary shift in the behavioural set-point as well.