Hypothalamic Thermosensitivity Research Articles

Effect of Long-Term Adaptation to Cold and Short-Term Cooling on the Expression of the TRPM2 Ion Channel Gene in the Hypothalamus of Rats

The present study is aimed to elucidate the possible involvement of the thermosensitive TRPM2 ion channel in changing of the temperature sensitivity of the hypothalamus after different cold exposures-long-term adaptation to cold and short-term cooling. Quantitative RT-PCR was used to study the expression of the gene of thermosensitive TRPM2 ion channel in the hypothalamus in the groups of control (kept for 5 weeks at +20 to +22 °C) and cold-adapted (5 weeks at +4 to +6 °C) rats, as well as in the groups of animals which were subjected to acute cooling (rapid or slow) with subsequent restoration of body temperature to the initial level. It has been shown that after long-term adaptation to cold, the decrease in the Trpm2 gene expression was observed in the hypothalamus, while a short-term cooling does not affect the expression of the gene of this ion channel. Thus, long-term adaptation to cold results in the decrease in the activity not only of the TRPV3 ion channel gene, as shown earlier, but also of the Trpm2 gene in the hypothalamus. The overlapping temperature ranges of the functioning of these ion channels and their unidirectional changes during the adaptation of the homoeothermic organism to cold suggest their functional interaction. The decrease in the Trpm2 gene expression may indicate the participation of this ion channel in adaptive changes in hypothalamic thermosensitivity, but only as a result of long-term cold exposure and not of a short-term cooling. These processes occurring at the genomic level are one of the molecular mechanisms of the adaptive changes.

Monitoring the development of thermoregulation in poultry embryos and its influence by incubation temperature

The general purpose of this review is to show the stage of the development of peripheral and central nervous thermoregulatory mechanisms in poultry embryos at the end of incubation, and the impact of long-term changes in incubation temperature. Methods are described which (a) allow continuous measurement of peripheral thermoregulatory mechanisms simultaneously with the body temperature of the embryo, and (b) can be used for identification of changes in the sensitivity of the central controller of body temperature during the development as well as after prenatal temperature experiences. Further, a method for characterisation of ‘critical periods’ in the development of the respective body function is introduced. The results of our investigations were discussed in relation to the following general rules: (a) The development of peripheral and central nervous thermoregulatory mechanisms begins in the course of the prenatal ontogeny. At the end of incubation poultry embryos have all the prerequisites to react to changes in incubation temperature. Regarding the peripheral thermoregulatory mechanisms the most sensitive parameter for characterization of the developmental level of embryonic thermoregulation is the deep body temperature. (b) Functional systems of the organism develop from open loop system without feedback control into closed system controlled by feedback mechanism. Acute changes in the environmental conditions (e.g. incubation temperature) induce as a rule, initially uncoordinated and immediately non-adaptive reactions. Later the uncoordinated (immediately non-adaptive) reactions change into coordinated (adaptive) reactions, probably with closing of the regulatory system (‘critical period’). Environmental manipulation of immature physiological mechanisms could be used for characterization of ‘critical periods’ of the respective system. Monitoring of changes in the reactions of thermoregulatory mechanisms on the applied changes in incubation temperature during different perinatal time windows could help to limit ‘critical periods’ in the development of the thermoregulatory system. (c) During this ‘critical periods’, the actual environment modulates the development of the respective physiological control systems for the entire life period. Perinatal epigenetic temperature adaptation could be a tool to adapt poultry embryos or hatchlings to later climatic conditions. For detection of immediate and long-term effects of perinatal epigenetic temperature adaptation (‘imprinting’ of the thermoregulatory system) recordings of changes in neuronal hypothalamic thermosensitivity as well as in neuronal response on temperature stress are useful and have to be verified by identification of the respective effector genes and epigenetic changes in its expression.

Ontogeny of avian thermoregulation from a neural point of view

The ontogeny of thermoregulation differs among (avian) species, but in all species both neural and endocrinological processes are involved. In this review the neural processes in ontogeny of thermoregulation during the prenatal and early postnatal phase are discussed. Only in a few avian species (chicken, ducklings) the ontogeny of some important neural structures are described. In the early post hatching phase, peripheral and deep-body thermoreceptors are present and functional, even in altricial species, in which the thermoregulation is still immature at hatch. It is suggested that the development of peripheral and deep-body thermoreceptors is not responsible for the inability to maintain a stable body temperature at cold ambient temperatures during early postnatal phase, although studies examined the ontogeny of thermoreception only in an indirect manner. Thus, other factors, such as volume to surface ratio and rate of insulation are important. Studies regarding the ontogeny of hypothalamic cold- and warm-sensitivity neurons in precocial species demonstrate that maturation of the hypothalamic temperature sensitivity takes place during the late prenatal and early postnatal period, with a relatively high cold sensitivity of the hypothalamus during the transition from poikilotherm to homeotherm. In addition, incubation temperatures are demonstrated to influence postnatal hypothalamic thermosensitivity. Brain temperature regulation is found to maturate during avian ontogeny as well and is demonstrated to coincide with the ontogenic pattern of general thermoregulation in several avian species. Relevant information of the ontogeny of the spinal cord and effector pathways related to the development of avian thermoregulation is lacking. We concluded that both prenatal and early postnatal temperature affects hypothalamic thermosensitivity and consequently condition thermoregulation in later life.

Pyrogenic effects of cytokines (IL-1β, IL- 6, TNF-α) and their mode of action on thermoregulatory centers and functions

The objective of this study was to compare the thermoregulatory responses of rabbits to fever-inducing doses of various cytokines (IL-1β, IL-6, TNF-α) injected peripherally (i.v.), or centrally (i.h.).TNF-α (1μgkg−1), when applied i.v. at thermoneutral conditions, induced a long lasting increase in hypothalamic temperature, which reached maximal values within 50min and then persisted for at least 3h. This monophasic fever-like response was due to extensive and long lasting attenuation of panting and due to transient vasoconstriction. Metabolic rate tended to increase during the early phase of the fever, only. On the other hand, IL-6 when applied i.v. in the same dose (1μgkg−1) and IL-1β, in a much lower dose (60ngkg−1), induced a short lasting monophasic hyperthermia due to transient attenuation of panting and due to transient vasoconstriction. No significant increase in metabolic rate was observed. The immediate attenuation of panting and induction of vasoconstriction rather resembled reflex (shock) responses than specific thermoregulatory reactions. Thirty minutes after i.v. administration of TNF-α, temperature thresholds for induction of cold thermogenesis, panting and vasomotion were shifted to higher body temperatures and remained elevated for at least 3h. In case of IL-1β the increased temperature thresholds were observed 30min after i.v. administration, only. I.v. applied IL-6 did not influence the thresholds neither 30 or 180min after injection. Thus, peripheral IL-6 rather induced hyperthermia than fever.When injected i.h. all cytokines studied induced a long lasting increase in body temperature similar to that after i.v. injection of LPS. Temperature thresholds for induction of all thermoregulatory outputs were increased and remained increased for at least 3h. No changes in hypothalamic thermosensitivity were observed. Data indicate a nonspecific effect of central cytokines on body temperature control.IL-1β appeared to be the most potent fever inducer. Nanogram doses of IL-1β injected i.v. induced a similar febrile response as microgram doses of other cytokines. On the other hand, TNF-α induced a longer lasting fever than other cytokines.

Early development of neuronal hypothalamic thermosensitivity in birds: influence of epigenetic temperature adaptation

The aim of the study was to investigate the prenatal influence of different incubation temperatures on the early postnatal development of neuronal hypothalamic thermosensitivity in birds. The experiments were carried out in brain slices of 1-, 5- and 10-days-old Muscovy ducklings incubated at 35, 37.5 (control) or 38.5 °C during the last week of incubation. Firing rate of neuronal activity was recorded extracellularly during sinusoidal temperature changes. The results show that the temperature experienced prenatally has a clear influence on postnatal neuronal hypothalamic thermosensitivity. For instance, at the 10th day post-hatching, exposure to the cooler prenatal incubation temperature resulted in elevated neuronal hypothalamic warm sensitivity through an increased proportion of warm sensitive neurons and a reduced proportion of cold sensitive neurons in comparison with the control group. Exposure to the warmer prenatal incubation temperature induced the opposite effect. In these age group changes in neuronal hypothalamic thermosensitivity occur in relation to the prenatal temperature experienced (proximate adaptive). During the first days of life, prenatal temperature load induced a significant change in the thermosensitivity of hypothalamic neurons which was independent of the direction of change in incubation temperature in comparison with control conditions (proximate non-adaptive). Changes in the thermosensitivity of hypothalamic neurons after prenatal temperature experiences observed in all age groups may be the result of epigenetic temperature adaptation.

Thermoregulation in Winter Swimmers and Physiological Significance of Human Catecholamine Thermogenesis

Thermoregulation in control subjects and cold-adapted winter swimmers was examined during 1 h of cold water immersion (13 C). It was found that the thermoregulatory functions of winter swimmers differ from those of non-cold-adapted subjects. As evident from the relationship between rectal temperature and the magnitude of cold thermogenesis, in controls a significant part of cold thermogenesis during the early phase of cooling was induced by changes in peripheral temperature input, while in the late phase of cooling it was the central temperature input which was mainly engaged in induction of cold thermogenesis. In winter swimmers the magnitude of cold thermogenesis was solely related to changes in rectal temperature, indicating the predominance of the central temperature input in activation of heat production mechanisms. The thermoregulatory threshold for induction of cold thermogenesis was lowered (by 0.34 C), but the apparent hypothalamic thermosensitivity was the same as in non-cold-adapted subjects. These differences are indicative of adaptation of thermoregulatory control centres. Additionally, the activity of thermoregulatory effectors was also changed. Shivering was induced later during cooling (after 40 min) in winter swimmers than in controls, which suggests an important participation of non-shivering thermogenesis in the early thermogenic response. Winter swimmers also showed bradycardia and a greater reduction in plasma volume during cooling. The data indirectly indicate restriction of heat loss from the body. Only a non-significant increase in quantity of subcutaneous fat was observed in winter swimmers. Thus, winter swimmers were able to survive a significantly greater temperature gradient between body and environment than non-cold-adapted subjects by modifying the sensory functions of hypothalamic thermoregulatory centres to lower heat loss and produce less heat during cold exposure. Additionally, the capacity of the total cold thermogenesis due to potentiation of non-shivering heat production was also increased. Heat produced due to thermogenic action of adrenaline may represent more than a quarter of the total cold thermogenesis. In conclusion, the data suggest that winter swimmers exhibit metabolic, hypothermic and insulative types of cold adaptation.

Influence of bombesin on neuronal hypothalamic thermosensitivity during the early postnatal period in the Muscovy duck ( Cairina moschata)

The influence of bombesin (1 μg/0.1 ml artificial cerebrospinal fluid) on neuronal thermosensitivity of the preoptic area of the anterior hypothalamus in brain slices of 5- ( n=7 neurons) and 10-day-old ( n=36 neurons) Muscovy ducks ( Cairina moschata) was investigated. Similar to adult mammals, most of the neurons investigated increased the firing rate (FR) after bombesin application. Changes in FR were not related to changes in thermal coefficient (TC). The neurons react to bombesin also under synaptic blockade. The bombesin-induced effect on TC (increase or decrease in nearly the same number of neurons, e.g. nine neurons increased and ten decreased TC in 10-day-old ducklings) in the postnatal bird neurons investigated was different from the results described in adult mammals, where the main reaction to bombesin was an increase of TC in warm-sensitive and temperature-insensitive-neurons and a transformation of temperature-insensitive-neurons into warm-sensitive ones. This may be related to the assumption that during early ontogeny, body functions react to exogenous and endogenous factors nonspecifically. It is to speculate, that later, probably at the end of embryonic development or during the early postnatal period, the reactivity of these functions changes qualitatively, so that the reaction of an individual function to different factors becomes specific (ultimately adaptive).

Chapter 3 Spinal neuronal thermosensitivity in vivo and in vitro in relation to hypothalamic neuronal thermosensitivity

In the spinal cord, temperature signals are generated which serve as specific inputs in the central nervous control of body temperature. Because of the spatially distinct organization of afferent and efferent neuronal systems at the spinal level, the afferent pathway for temperature signal transmission could be identified in vivo in the ascending, anterior and lateral tracts with a relationship of about 75:25% between warm and cold sensitive neuraxons. Analysis of spinal neuronal thermosensitivity in vitro on spinal cord tissue slices has been concerned, so far, with the superficial laminae of the dorsal horn as the site of origin of ascending nerve fibers conveying mostly temperature and pain signals, and with lamina X as a site of origin of afferent as well as efferent neurons. A relationship of about 95:5% between warm and cold sensitive neurons was found at the segmental level, indicating that warm sensitivity is the prevailing, primary property of spinal neurons, whereas cold sensitivity seems to be mainly generated by synaptic interaction as a secondary modality. Dynamic responses to temperature changes were frequently displayed in vitro at the spinal segmental level in lamina I + II but not in lamina X, even by neurons whose static activity was little influenced by local temperature. Dynamic thermosensitivity was found less frequently in ascending tract neuraxons and was not observed in hypothalamic neurons receiving temperature signal inputs from the spinal cord, and thus, does not seem to be relevant for the thermosensory function of spinal cord neurons, unlike peripheral warm and cold receptors. A majority of spinal warm sensitive neurons displayed both static and dynamic warm sensitivity as an inherent property after synaptic blockade. In the further analysis of spinal cord thermosensitivity, the in vitro approach permits application of the same electrophysiological and neuropharmacological methods as were established for the analysis of hypothalamic thermosensitivity. In addition, the topography of the spinal cord will provide additional structural and possibly histochemical information to characterize the functions of neurons independently of their thermal properties.

Neuropeptides and the central regulation of body temperature during fever and hibernation

Neuropeptides, acting on structures within the central nervous system influence body temperature. Non-opioid peptides induce hypothermia usually, while opioid peptides are mostly hyperthermic. Neuropeptides exert their effect only when injected into specific brain areas. Hypo- Or hyperthermic effect of neuropeptides may be either due to changes in threshold body temperatures for induction of thermoregulatory effectors or due to changes in hypothalamic thermosensitivity. At the cellular level the opioid peptides also act differently than the non-opioid peptides. The opioid peptides mostly inhibit spontaneous neuronal firing, while the non-opioid peptides usually stimulate it. Neuropeptides exert their influence on all neurones in the hypothalamus, independently on their temperature characteristics. Neuropeptides may play a role in the regulation of body temperature under stressful conditions and during fever or hibernation, in particular. Some neuropeptides, namely AVP, α-MSH and ACTH, act as natural antipyretic substances by lowering the threshold for cold thermogenesis. Neuropeptides also modulate food intake, reproduction and many other functions which are substantially changed during hibernation. There appears to be a correlation between the effect of peptides on the control of food intake and on the control of body temperature. Opioid peptides, which increase food intake, induce hyperthermia, while non-opioid peptides, which are appetite inhibiting, induce hypothermia. The exact role o neuropeptides in the regulation of body temperature, food intake and gonadal activity of hibernators remains unclear, however.

Sleep and hypometabolism

Metabolic rate (MR) of endotherms is lower during sleep than quiet wakefulness (W), largely as a result of a regulated lowering of body temperature (Tb) during slow-wave sleep (SWS). In mammals this decrease in regulated Tb is evidenced by a lowered hypothalamic thermosensitivity. In avian thermoregulatory systems spinal thermosensitivity is lower in SWS than in W. In rapid eye movement sleep (REMS) there is a severe inhibition of the thermoregulatory systems. Hypothalamic cells that are thermosensitive during W become less so during SWS and become totally insensitive to temperature during REMS. The adjustments in thermoregulatory systems of endotherms that result in lower Tb and MR during SWS have been shaped by natural selection in different species to produce a variety of adaptations for energy conservation. Bouts of torpor, hibernation, or nocturnal hypothermia consist mostly of SWS, and these states involve a downward resetting of hypothalamic thermosensitivity in mammals and spinal thermosensitivity in birds. A physiological mechanism underlying this change in regulation of Tb may be related to the regulation of breathing and acid–base balance. Retention of CO2 occurs at the onset of sleep, shallow torpor, and hibernation and release of excess CO2 occurs when these states are reversed by arousal. Increased plasma CO2 may have a direct effect on hypothalamic neurons involved in thermoregulation, resulting in a decline in regulated Tb.

Thermoregulatory responses of febrile sheep to spinal and hypothalamic heating.

Fever was induced by the intravenous injection of 0.25 microgram/kg of lipopolysaccharide (LPS) from Escherichia coli in eight conscious sheep exposed to ambient temperatures adjusted to the lower range of thermoneutrality. Chronic spinal or hypothalamic thermodes were perfused with water of 44 degrees C for 20 min or for most of the rising phase of fever (100 min of the mean 166 min total rise time). The effects of spinal and hypothalamic heating were identical. Thus, before LPS, spinal or hypothalamic heating did not affect the rate of O2 consumption (VO2) but increased skin blood flow (as indicated by skin temperatures) and elicited panting; therefore rectal temperature (Tre) fell. During fever rise, the already reduced skin blood flow and respiratory rate were not affected by spinal or hypothalamic heating, but the increased VO2 was reduced; consequently, the rise in Tre was attenuated. During the plateau phase of fever, all responses were similar to those seen before LPS. In febrilysis, heating strongly enhanced the operating heat loss mechanisms and, hence, augmented the fall in Tre. Thus, although the thermoeffectors activated by spinal or hypothalamic heating were modified during the different stages of fever, the effect on body temperature was nearly the same. Therefore there seems to be no change in spinal or hypothalamic thermosensitivity during fever in sheep.

Appropriate and inappropriate hypothalamic cold thermosensitivity in Willow ptarmigan.

Hypothalamic thermosensitivity has been investigated in conscious Willow Ptarmigan (Lagopus lagopus lagopus) provided with chronically implanted hypothalamic perfusion thermodes. The birds were exposed to either cold (Ta - 10 degrees C) or warm (Ta + 25 degrees C) ambient conditions while hypothalamic temperature (Thy) was clamped for periods of 20 min at different set levels between 28 degrees C and 43 degrees C. The responses of the animals to hypothalamic thermal stimulation were classified by comparing them with those normally found in mammals. At Ta - 10 degrees C hypothalamic heating inhibited ongoing shivering, causing a fall in body-core temperature (Tc) (appropriate mammalian-like response). Strong levels of hypothalamic cooling (Thy less than 34.0 degrees C) also caused a fall in Tc due to inhibition of shivering (inappropriate mammalian-like response). However, weaker levels of hypothalamic cooling (Thy 34-36 degrees C), facilitated ongoing shivering, resulting in small increases in Tc (appropriate mammalian-like response). At Ta + 25 degrees C hypothalamic heating facilitated ongoing panting while weak (Thy 38 degrees C) levels of hypothalamic cooling inhibited ongoing panting (both mammalian-like responses). The observation of a weak mammalian-like cold hypothalamic thermosensitivity in Willow Ptarmigan indicates that these birds possess some specific cold thermosensors in the hypothalamic region. This finding suggests that hypothalamic temperature dependence in birds and mammals is fundamentally similar.

Effects of selective cutaneous denervation on hypothalamic thermosensitivity in rats

The effect of altering input from cutaneous thermoreceptors of the face and trunk on the relationship between hypothalamic temperature (Thy) and heat production (HP) was studied in three rats. The signal from cutaneous receptors was altered in two ways: by altering skin temperature (Tsk) and by sectioning nerves supplying cutaneous receptors. It was found that when Tsk was lowered in normal rats Thy threshold for thermoregulatory HP was elevated, but the slope of the relationship between Thy and HP was not significantly altered. After the spinal nerves serving the trunk skin were sectioned, the slope was reduced and the threshold was elevated markedly at both test ambient temperatures (Ta), but Ta had essentially the same effect on the Thy vs. HP relationship after cutaneous denervation as before. Clearly, eliminating input from trunk cutaneous thermoreceptors has a different effect than does lowering or raising Tsk, but thermoregulation is being achieved by the same basic mechanism before and after cutaneous denervation. After the cranial nerves supplying the skin of the face were also sectioned, there was a further elevation in the Thy threshold for HP at Ta = 25 degrees C but no change at Ta = 15 degrees C. It is concluded that cutaneous denervation does not substantially interfere with the rat's ability to regulate its body temperature, and that the reduced Thy sensitivity and increased Thy threshold exhibited after cutaneous denervation is the result of input from intact warm- and cold-thermoreceptors located in the core and in tissues intermediate to core and skin.

Hypothalamic thermosensitivity in capsaicin-desensitized rats.

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.

Central control of expired air temperature and other thermoregulatory effectors in reindeer.

Norwegian reindeer (Rangifer tarandus tarandus) were provided with chronically implanted hypothalamic perfusion thermodes to determine to what extent expired air temperature (Tex) is centrally controlled. The effects that alterations of hypothalamic temperature (Thy) had on metabolic heat production, respiratory frequency, respiratory evaporative heat loss, and rectal and leg-skin temperature were simultaneously recorded. Experiments were conducted in conscious animals exposed to ambient temperatures (Ta) of -20, 0, and 20 degrees C in summer, when fur insulation was minimal, and in winter, when it was prime. Altering Thy induced changes in Tex, the degree and direction of which depended on the prevailing Ta, season, and intensity of hypothalamic thermal stimulation. These results indicate that Tex, and hence nasal heat exchange, is under central control. The Thy-induced changes in the other measured parameters confirm that hypothalamic thermosensitivity in these animals is similar to that previously found in other mammalian species.

Reduced hypothalamic thermosensitivity following intraventricular injection of pyrogen in conscious rabbits

Hypothalamic temperature thresholds for vasodilatory and respiratory reactions were determined before and after i.c.v. injection of pyrogen in rabbits. During the rising phase of fever the increases in the hypothalamic thresholds for vasodilatory and respiratory reactions differed from those found in the pre-pyrogen preoptic anterior hypothalamic area (POAH) heating by2.1 ± 0.2°C and1.89 ± 0.31°C, respectively. During the plateau phase of fever the threshold for vasodilatory raction was further increased (by0.7 ± 0.23°C), whereas that for panting remained at the same level. It is concluded that pyrogen exerts a depressive action on POAH thermosensitivity.

Hypothalamic thermosensitivity in an Emu, Dromiceius Novae-Hollandiae.

Thermosensitivity of the rostral brainstem was tested in a conscious Emu which had been previously implanted with a hypothalamic perfusion thermode. Hypothalamic warming decreased colonic temperature and cooling increased it. The maximum response to cooling occurred at a hypothalamic temperature of 34.4 °C and was accompanied by visible shivering. Thus in the Emu specific hypothalamic thermosensitivity appears to extend, relative to that in other avian species, further down into the hypothermic range, to some extent resembling the mammalian type of brainstem thermosensitivity.

Effects of CNS temperature on generation and transmission of temperature signals in homeotherms. A common concept for mammalian and avian thermoregulation.

Neurophysiological studies on avian hypothalamic thermosensitivity have presented evidence for a higher Q10 of cold than of warm signal transmission in the CNS of birds. An identical temperature dependence of central cold and warm signal transmission in mammals is suggested by considerations on the phylogeny of temperature regulation. By taking into account the experimental evidence for the existence of thermosensory afferents in the CNS of mammals and birds, being differently developed in the various sections of the neural axis and exerting quantitatively different influences on the various thermoregulatory effectors, a common concept of homeothermic thermoregulation is proposed resting on the same basic assumptions for mammals and birds. The great diversity of negative as well as positive feedback effects of CNS temperature displacements on homeothermic thermoregulation, which is particularly expressed in avian autonomic and behavioral thermoregulation and, further, certain pathophysiological conditions of disturbed thermoregulation could be accounted for by assuming quantitatively different contributions of the central thermosensory inputs of thermoregulatory effector control, but maintaining the Q10 values of hypothalamic warn and cold signal transmission constant. The proposed model, while basically additive in its mathematical design, meets a number of properties described by multiplicative models of thermoregulation. In additionally generalizes these models of predicting that changes of hypothalamic temperature modify the sensitivities with which any thermoregulatory effector responds to any thermosensory input.

Thermal control of respiratory evaporative heat loss in exercising dogs.

Experiments were carried out to determine whether respiratory evaporative heat loss (REHL) in exercising dogs is entirely under thermal control or whether a nonthermal input is additionally involved. To determine body core thermosensitivity, hypothalamic perfusion thermodes and intravascular heat exchanges were chronically implanted in the animals. This allowed the temperature of these two areas to be independently manipulated. At 30 degrees C air temperature, REHL was measured in three dogs during rest or while running on a treadmill (6 km . h-1, 0 degree gradient). During exercise, the threshold temperature was lowered by 9 degrees C, and the slope of the heat-loss response was reduced to one-third as compared with rest when hypothalamic temperature alone was clamped at various levels between 30 degrees and 42 degrees C. However, when extrahypothalamic body core temperature was additionally clamped, the decrease in threshold during exercise was reduced to 0.43 degrees C, while the slope of the response was identical to that during rest. The results suggest that by taking account of total body core thermosensitivity, instead of hypothalamic thermosensitivity, the alleged role of a nonthermal input is greatly reduced. In addition, the results showed that the major pat of central thermosensitivity must be attributed to the extrahypothalamic body core.

Hypothalamic thermosensitivity in conscious Pekin ducks.

Conscious Pekin ducks with chronically implanted hypothalamic thermodes were submitted to thermoneutral (Ta 25 degrees C), cold (Ta 5 degrees C), and warm (Ta 33 degrees C) ambient temperatures. Hypothalamic temperature (Thy) was varied in nine steps between 27.9 and 43.5 degrees C in repeated experiments. Cooling of the hypothalamus induced a fall of core temperature (Tc) that was linearly related to Thy and amounted to 1.1--1.3 degrees C at highest cooling intensity. The decrease of Tc was caused by inhibition of metabolic heat production and/or vasodilatation in the skin at cold and thermoneutral Ta and by activation of panting at warm Ta. After the end of cooling a temporary overshoot of heat production occurred, the degree of which depended on the degree of cooling and on Ta, and led to a rapid normalization of Tc. Warming of the hypothalamus induced a slight fall of Tc due to a reduction of metabolic heat production at cold and thermoneutral Ta and to an activation of panting at warm Ta. It is concluded that no specific cold reception and a weak specific warm reception exist in the duck's hypothalamus. A "nonsensory" temperature susceptibility of hypothalamic control functions is responsible for those reactions of thermoregulatory effector activities which do not fall into the categories of adequate thermoregulatory responses to a central thermal stimulus.