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We examined effects of the queen's presence on diurnal rhythms of temperature preference (TP) and locomotor activity (LA) in worker honeybees' groups. TP and LA of six queenless and six queenright (with the queen) groups of bees, consisting of 7-8 worker bees, were recorded in a thermal gradient system for four days, under light to darkness (LD) 12:12 photoperiod. The same experiments were conducted on five virgin queens (of the same age as those in the queenright groups), which were placed individually in the gradient chambers. The single virgin queens showed signs of distress and no rhythms of TP and LA. In contrast, there were diurnal rhythms of TP and LA in both group variants with daytime activity and nighttime rest. However, the queen's presence exerted a strong calming effect, reducing LA of bees both at day- and nighttime. The nighttime minimum LA of queenright groups was five times lower than that in queenless groups. Moreover, there was a reversal of the diurnal pattern of TP in queenright groups. The results are discussed in terms of the bee colony organization as a superorganism.

Thermoregulation in patients suffering from multiple sclerosis (MS) is impaired and may result in either increases or decreases in body temperature. We have found that rat experimental autoimmune encephalitis (EAE), being a model of MS, is associated with body temperature disturbances as well. The purpose of the current study was to examine whether the altered body temperature in EAE-induced rats is due to either a deficit in thermoregulation or a controlled change in its set point. Subcutaneous injection of encephalitogenic emulsion into both pads of hind feet of the Lewis rats provoked EAE symptoms. Body temperature (Tb) of 6 rats was measured using biotelemetry system, and ambient temperature (Ta) preferred by 6 rats of another group was analyzed using thermal gradient system. Symptoms of EAE started 11 days postinjection and progressed quickly, culminating in a complete paralysis in rats placed in the gradient, which was associated with behavioural fever (accordingly, selected Ta raised to as much as 32.8 ± 0.5 °C vs 27.2 ± 0.6 °C in control rats). On the other hand, EAE rats, placed at a constant Ta of 24 °C, were able to generate fever (Tb of 37.8 ± 0.1 °C) at the start of the illness and then paralysis compromised fever (most likely due to an impairment of thermogenesis), which, surprisingly, resulted in recovery. We conclude that EAE onset in rats is associated with fever and its behavioural supporting leads to aggravation of the autoimmune neurotoxicity., (Copyright © 2020 Nicolaus Copernicus University, ToruD, Poland. Published by Elsevier Ltd.. All rights reserved.)

After hypoxic-ischemic insult iron deposited in the brain catalyzes formation of reactive oxygen species. Newborn rats, showing reduced physiological body temperature and their hyperthermic counterparts injected with deferoxamine (DF), a chelator of iron, are protected both against iron-mediated neurotoxicity and against depletion of low-molecular antioxidants after perinatal asphyxia. Therefore, we decided to study the effects of DF on activity of antioxidant enzymes (superoxide dismutase-SOD, glutathione peroxidase-GPx and catalase-CAT) in the brain of rats exposed neonatally to a critical anoxia at body temperatures elevated to 39°C. Perinatal anoxia under hyperthermic conditions intensified oxidative stress and depleted the pool of antioxidant enzymes. Both the depletion of antioxidants and lipid peroxidation were prevented by post-anoxic DF injection. The present paper evidenced that deferoxamine may act by recovering of SOD, GPx and CAT activity to reduce anoxia-induced oxidative stress., (Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.)

It is well known that decrease in body temperature provides protection to newborns subjected to anoxia/ischemia. We hypothesized that the normal body temperature of 33°C in neonatal rats (4°C below normal body temperature in adults) is in fact a preadaptation to protect CNS from anoxia and further reductions as well as elevations in temperature may be counterproductive. Our experiments aimed to examine the effect of changes in body temperature on oxidative stress development in newborn rats exposed to anoxia. Two-day-old Wistar rats were divided into 4 temperature groups: i. hypothermic at body temperature of 31°C, ii. maintaining physiological neonatal body temperature of 33°C, iii. forced to maintain hyperthermic temperature of 37°C, and i.v. forced to maintain hyperthermic temperature of 39°C. The temperature was controlled starting 15 minutes before and afterword during 10 minutes of anoxia as well as for 2 hours post-anoxia. Cerebral concentrations of lipid peroxidation products malondialdehyde (MDA) and conjugated dienes (CD) and the activities of antioxidant enzymes had been determined post mortem: immediately after anoxia was finished and 3, 7, and 14 days later. There were no post-anoxic changes in the concentration of MDA, CD and in antioxidant enzymes activity in newborn rats kept at their physiological body temperature of 33°C. In contrast, perinatal anoxia at body temperature elevated to 37°C or 39°C as well as under hypothermic conditions (31°C) intensified post-anoxic oxidative stress and depleted the antioxidant pool. Overall, these findings suggest that elevated body temperature (hyperthermia or fever), as well as exceeding cooling beyond the physiological level of body temperature of newborn rats, may extend perinatal anoxia-induced brain lesions. Our findings provide new insights into the role of body temperature in anoxic insult in vivo.

Hypoxic-ischaemic brain injury involves increased oxidative stress. In asphyxiated newborns iron deposited in the brain catalyses formation of reactive oxygen species. Glutathione (GSH) and vitamin E are key factors protecting cells against such agents. Our previous investigation has demonstrated that newborn rats, showing physiological low body temperature as well as their hyperthermic counterparts injected with deferoxamine (DF) are protected against iron-mediated, delayed neurotoxicity of perinatal asphyxia. Therefore, we decided to study the effects of body temperature and DF on the antioxidant status of the brain in rats exposed neonatally to critical anoxia. Two-day-old newborn rats were exposed to anoxia in 100% nitrogen atmosphere for 10 min. Rectal temperature was kept at 33 °C (physiological to rat neonates), or elevated to the level typical of healthy adult rats (37 °C), or of febrile adult rats (39 °C). Half of the rats exposed to anoxia under extremely hyperthermic conditions (39 °C) were injected with DF. Cerebral concentrations of malondialdehyde (MDA, lipid peroxidation marker) and the levels of GSH and vitamin E were determined post-mortem, (1) immediately after anoxia, (2) 3 days, (3) 7 days, and (4) 2 weeks after anoxia. There were no post-anoxic changes in MDA, GSH and vitamin E concentrations in newborn rats kept at body temperature of 33 °C. In contrast, perinatal anoxia at elevated body temperatures intensified oxidative stress and depleted the antioxidant pool in a temperature-dependent manner. Both the depletion of antioxidants and lipid peroxidation were prevented by post-anoxic DF injection. The data support the idea that hyperthermia may extend perinatal anoxia-induced brain lesions.

During summer, land snails are exposed to estivation/arousal cycles that imposes oxidative stress, but they exhibit different patterns of antioxidant defence. To test the ability of two related species, Helix pomatia and Helix aspersa, to modulate their antioxidant defence mechanism during estivation/arousal cycles, we examined activities of catalase and glutathione-related enzymes and concentrations of glutathione and thiobarbituric acid reactive substances (TBARS; as products of lipid peroxidation). In both species, estivation evoked changes in activity of total and selenium-dependent glutathione peroxidase (GPx), but did not affect activity of catalase, glutathione reductase, and glutathione transferase, and had no effect on concentration of glutathione. Activity of catalase in estivating snails, instead of the expected increase, showed a tendency to diminish. Extremely low activities of catalase in the foot were usually associated with extremely high activities of both forms of GPx. In conclusion, maintenance of relatively high activities of the antioxidant enzymes and accumulation of glutathione, resulting in a low and stable concentration of TBARS, plays an important role in scavenging oxygen free radicals from the organism of both species., (2011 Wiley Periodicals, Inc., A Wiley Company.)

Neonatal anoxia is an example of early-life threatening experience that might exert long-lasting behavioral disturbance. One of the consequences of neonatal asphyxia is hyperactivity in open-field test. Changes in open-field activity are coupled with changes in the function of the hypothalamic-pituitary-adrenal (HPA) axis. A critical determinant of the severity of hypoxic-ischemic brain injury in newborn rats is body temperature. Hyperthermia under anoxic conditions increases locomotor activity in the open-field test. Therefore, the aim of the present study was to test whether body temperature during neonatal anoxia can affect basal and stress-induced corticosterone secretion in rats. At the age of 2 days Wistar rat pups were exposed to anoxia in 100% nitrogen atmosphere. Rectal temperature was kept at 33 degrees C (typical for the rat pups), or was elevated to a level typical for febrile adults (39 degrees C). Control rats were exposed to atmospheric air under the respective thermal conditions. Basal and stress-induced corticosterone levels were assessed using sulphuric acid-induced fluorescence, on postnatal day 14. Body temperature during neonatal asphyxia altered the early developmental profile of plasma corticosterone. Hyperthermia under anoxic conditions decreased the corticosterone response to open-field stress. In conclusion, febrile body temperature changes corticosterone release, which might induce neurobehavioral disturbances. On the other hand, a protection against the HPA dysfunction can be achieved by the reduced physiological neonatal body temperature., (Copyright 2010 Elsevier Ireland Ltd. All rights reserved.)

Estivation enables land snails to survive a prolonged dryness but the return to active state imposes conditions of oxidative stress on internal organs due to a transient large increase in oxygen consumption, which augments mitochondrial production of reactive oxygen species. Therefore, activities of antioxidant enzymes, concentrations of reduced glutathione (GSH) and TBARS as an index of lipid peroxidation, were evaluated in Helix pomatia snails (i) during summer activity, (ii) during estivation, which was induced experimentally, (iii) at the start of arousal from estivation, and (iv) being aroused for 24 h. Estivation induced significant decreases in activity of catalase in the kidney and hepatopancreas and glutathione peroxidase in the kidney. Activity of glutathione reductase was unaffected by estivation/arousal cycle. Summer-active and estivating snails maintained high activity of glutathione transferase. Concentration of GSH was organ-dependent and was positively affected by estivation. Lack of increase in TBARS concentration during estivation/arousal cycle suggests that antioxidant defence system of H. pomatia snails is highly efficacious. In conclusion, permanent maintenance of relatively high activities of the antioxidant enzymes and the high concentration of GSH in H. pomatia snails indicate that they have well-developed strategy of defence against oxidative injury.

Terrestrial snails are often exposed to freezing. Therefore, we investigated seasonal shifts in hemolymph concentrations of cryoprotectants such as glycerol and glucose. We also investigated whether summer acclimation to cold and short-day photoperiod induced synthesis of cryoprotectants in Helix pomatia snails. Concentrations of the both cryoprotectants were elevated in winter and reduced in summer. These changes, however, were not correlated with shifts in liver glycogen content. Summer acclimation to cold (5 degrees C) and short-day photoperiod evoked a selective increase in glycerol concentration. In conclusion, glycerol may play a role in adaptation of the snails to winter cold and glucose is rather unlikely to provide the cryoprotection.

Various animals must cope with some specific extreme environmental conditions and, as a consequence, they developed extremely efficacious adaptive defence responses. The mechanisms of the specific defences are more clearly visible in some species than in humans. Therefore, animal models of the human defence mechanisms should be selected accordingly. The appropriate, well responding models may be regarded as "biological amplifiers". This review is focussed on examples of effective defence against: (i) parturitional asphyxia, which extends fertility of mammals; (ii) diving asphyxia, which extends access of food in aquatic birds and mammals; (iii) endotoxemia, which provides survival of the fittest in mammals showing top fertility; (iv) deep hypothermia, which enables hibernating mammals to arouse. Each of the defences needs close co-operation of the cardiovascular, respiratory and temperature regulatory systems. Underlined problems regarding a choice of appropriate experimental animal models should stimulate renaissance of comparative physiology.

Perinatal asphyxia in mammals leads to iron accumulation in the brain, which results in delayed neurobehavioural disturbances, including impaired learning and abnormal alertness over their entire life span. The aim of this investigation was to verify our hypothesis that newborn rats, showing reduced normal body temperature, are protected against neurotoxicity of the asphyxia up to senescence. Alertness was studied in adult and old male Wistar rats after exposure to critical neonatal anoxia: (i) at physiological neonatal body temperature of 33 degrees C, (ii) at body temperature elevated to 37 degrees C, or (iii) at body temperature elevated to 39 degrees C (the thermal conditions remained unchanged both during anoxia and for 2 h postanoxia). To elucidate the effect of iron-dependent postanoxic oxidative damage to the brain, half of the group (iii) was injected with deferoxamine, a chelator of iron. Postanoxic behavioural disturbances were recorded in open-field, elevated plus-maze, and sudden silence tests when the rats reached the age of 12 and 24 months. Open-field stress-induced motor activity was reduced in rats subjected to neonatal anoxia under hyperthermic conditions. In contrast, these rats were hyperactive in the plus-maze test. Both the plus-maze and sudden silence tests show reduced alertness of these rats to external stimuli signalling potential dangers. The behavioural disturbances were prevented by body temperature of 33 degrees C and by administration of deferoxamine.

In asphyxiated newborns iron, released from heme and ferritin and deposited in the brain, contributes to neurodegeneration. Because hypothermia provides neuroprotection, newborn mammals, showing spontaneously reduced body temperature, might avoid the iron-mediated neurotoxicity. Therefore, we decided to study the effects of body temperature and chelation of iron with deferoxamine on iron accumulation in the brain of three weeks old rats exposed neonatally to a critical anoxia. At the age of two days, newborn rats were exposed to anoxia in 100% nitrogen atmosphere. Rectal temperature was kept at 33 degrees C (typical of the rat neonates), or elevated to a level typical of febrile (39 degrees C) adults. Control rats were exposed to atmospheric air in the respective thermal conditions. Half of the rats exposed to anoxia under hyperthermic conditions were injected with deferoxamine (DF), immediately after anoxia and 24 h later. Regional changes in cerebral iron deposition were examined in the frontal cortex, the hippocampus and the striatum, using iron histochemistry, when the rats reached the age of three weeks. Increased iron staining was found in neurons of each of the three cerebral regions in rats exposed to neonatal anoxia under hyperthermic conditions and the iron accumulation was prevented by postanoxic DF injection. In conclusion, febrile body temperature amplifies cerebral hyperferremia, which might induce neurodegenerative disturbances in the brain. On the other hand, a protection against the brain hyperferremia can be achieved by both the reduced physiological neonatal body temperature and by postasphyxic DF administration.

Alertness was studied in adult male Wistar rats after neonatal critical anoxia applied under three different thermal conditions: (i) at physiological neonatal body temperature of 33 degrees C, (ii) at body temperature elevated to 37 degrees C, and (iii) at body temperature elevated to 39 degrees C (both during anoxia and for 2 h postanoxia). To elucidate the effect of iron-dependent postanoxic oxidative damage to the brain, half of the group (iii) was injected with deferoxamine, a chelator of iron. Postanoxic behavioural disturbances were recorded in open-field, elevated plus-maze, and sudden silence tests when the rats reached the age of 4 month. Moreover, spontaneous motor activity of the rats was recorded radiotelemetrically in their home-cages. Both open-field stress-induced and spontaneous motor activity were reduced in rats subjected to neonatal anoxia under hyperthermic conditions. In contrast, these rats were hyperactive in the plus-maze test. Both the plus-maze and sudden silence tests revealed that these rats show reduced alertness to external stimuli signalling potential dangers. The behavioural disturbances were prevented by the body temperature of 33 degrees C and by postanoxic administration of deferoxamine. These data support the conclusion that permanent postanoxic behavioural disturbances are due to iron-dependent oxidative damage to the brain, which can be prevented by the reduced neonatal body temperature.

To study the relationship between the individual and social thermoregulatory behaviour, we used honeybee workers and American cockroaches. Single insects or groups of 10-20 individuals were placed in a temperature gradient chamber, and their thermal preference was recorded for 48 h under natural summer photoperiod. Single bees showed diurnal changes in selected ambient temperature, which culminated at 14:00 reaching 34+/-2 degrees C, and then slowly decreased, reaching a nocturnal minimum of 28+/-2 degrees C at 04:00. In contrast, the zenith of temperature selected by groups of bees (31+/-1 degrees C) was reached at 04:00 and the nadir (29+/-2 degrees C) was recorded at 14:00. Groups of bees clustered together during the night time, and dispersed during intense day time activity. Such changes were absent in groups of cockroaches. Cockroaches selected an ambient temperature of 30+/-1 degrees C both during day and night. In conclusion, there is a striking analogy in the diurnal thermal behaviour between a colony of bees and mammals. During their nychthemeral rest phase, both of them select higher temperatures than during the activity phase and, simultaneously, they reduce their overall surface area of heat loss to conserve metabolic heat. Therefore, the colony behaves as a homeothermic superorganism. In contrast, a single bee, isolated from the colony, utilizes a heterothermic strategy to save energy for a morning warm up.

Newborn mammals, showing reduced normal body temperature, might be protected against iron-mediated, delayed neurotoxicity of perinatal asphyxia. Therefore, we investigated the effects of (1) neonatal body temperature and neonatal critical anoxia as well as (2) postanoxic chelation of iron with deferoxamine, on open-field stress-induced behaviour in juvenile rats. The third aim of this study was to compare (after the above-mentioned treatments) circadian changes in spontaneous motor activity and body temperature in juvenile rats permanently protected from any stress. Neonatal anoxia at body temperature adjusted (both during anoxia and 2 h reoxygenation) to a level typical of healthy (37 degrees C) or febrile (39 degrees C) adults led to the stress-induced hyperactivity in juvenile (5-45 days old) rats. Both normal neonatal body temperature of 33 degrees C and chelation of iron prevented the hyperactivity in rats. Neither neonatal body temperature nor neonatal anoxia affected spontaneous motor activity or body temperature of juvenile rats, recorded in their home-cages with implantable transmitters. Circadian rhythmicity was also undisturbed. Presented data support the hypothesis that physiologically reduced neonatal body temperature can provide a protection against iron-mediated postanoxic disturbances of behavioural stress responses in juvenile rats.

Severe hyperthermia disrupts the intestinal barrier, allowing bacterial lipopolysaccharides (LPS) to enter the bloodstream. Since the symptoms of heat stroke resemble those of endotoxic shock, there is a common belief that endotoxaemia induces heat stroke. Therefore, we studied the effects of different doses, from moderate to sublethal, of Escherichia coli LPS and an antipyretic (indomethacin) upon the temperature equilibrium of the brain and body of rats exposed to a constant ambient temperature of 38 degrees C. The animals were then heated until they developed heat stroke, which was identified using a critical thermal maximum (CTM) behavioural test. In separate experiments on defence against endotoxaemia, we compared plasma lipid composition in rats exposed to a sublethal dose of LPS, hyperthermia and heat stroke. Neither LPS nor indomethacin, injected into rats while they were in a hyperthermic steady-state condition of 40-41 degrees C, influenced their thermal equilibrium. Unexpectedly, moderate doses of LPS significantly elevated the thermal tolerance of rats, such that the mean (SEM) CTM value of body temperature was raised from 42.7 (0.3) degrees C to 43.1 (0.1) degrees C (P < 0.05). Indomethacin and huge doses of LPS failed to induce any change in this parameter. The sublethal dose of LPS did not induce mortality in rats subjected to heat stroke. Hyperthermic steady-state conditions and heat stroke alone significantly decreased plasma concentrations of cholesterol, triglyceride and high-density lipoproteins, while the concentrations of low-density lipoproteins increased. A similar pattern of changes was recorded in normothermic rats injected with a sublethal dose of LPS. In conclusion, endotoxaemia in heat-stressed rats induces neither a secondary increase in their core temperature nor a decrease in their ultimate thermal tolerance. Low-density lipoproteins are likely to protect heat-stressed animals against endotoxin-induced death.

Hypothermia may limit asphyxic damages to the brain, and many small homeotherms have been shown to use anapyrexic strategies when exposed to asphyxic conditions. Larger homeotherms do not seem to use the same strategy, but could save oxygen and prevent hypoxic brain damage by employing selective brain cooling (SBC) in connection with asphyxia. To test the hypothesis that selective brain cooling may take place in connection with asphyxia, we have recorded brain [hypothalamic (THyp)] and body [colonic (TC)] temperatures and heart rates in four Pekin ducks during 5-min simulated (head submersion) diving in cold water (10 degrees C). Diving resulted in a drop in THyp (3.1 +/- 1.4 degrees C) that continued into the recovery period (P < 0.001). Restricting heat loss from the buccal cavity and eyes during diving compromised brain cooling in an additive manner. TC was not influenced by diving. Control cooling of the head with crushed ice during a 5-min period of undisturbed breathing had no effect on THyp. Warm water (35 degrees C) markedly reduced brain cooling, and dive capacity was reduced by approximately 14% (P < 0.05) compared with diving in water at 10 degrees C. The data suggest that SBC is used in ducks during diving, and we propose that this mechanism may enable the bird to save oxygen for prolonged aerobic submergence and to protect the brain from asphyxic damages.

The purpose of our study was a comparison of pyrogenic and behavioural effects of Escherichia coli (E.coli) and Salmonella abortus (S.abortus) endotoxins in unrestrained, freely moving Wistar rats, placed in a thermal gradient and having an easy access to ambient temperatures within a range 5-40 degrees C. Hypothalamic and chosen by the rats ambient temperatures as well as locomotor activity were recorded before and after intraperitoneal injection of 1 mg/kg lipopolysaccharide from E. coli or from S. abortus. Control animals were injected with pyrogen-free saline. Both endotoxins induced warm-seeking behaviour which was accompanied by biphasic fever. Locomotor activity of LPS-injected rats was reduced. S. abortus-induced fever peaked at 100th minute (reaching 37.5 +/- 0.2 degrees C) and at 250th minute (reaching 38.1 +/- 0.1 degrees C). Respective data for E. coli fever were: 170th minute (when hypothalamic temperature reached 37.6 +/- 0.3 degrees C) and 430th minute (with hypothalamic temperature of 38.6 +/- 0.1 degrees C). Comparing to S. abortus-generated fever both peaks of E. coli LPS-induced fever were significantly delayed (p < 0.05). A limited structural variability of lipid A from both bacteria is likely to be responsible for the difference in fever timing recorded in this study.