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E Briese

Publications and source records attributed to E Briese.

At least 19 recordsLinked to original sources
PubMed1998

Normal body temperature of rats: the setpoint controversy.

Emotional hyperthermia, circadian variations and the rise of body temperature related to exercise, have all been attributed to setpoint temperature shifts. The accepted theory holds that core temperature is regulated by corrective thermoregulatory responses opposing the core temperature deviations from the setpoint level. However, in fever and anapyrexia the thermoregulatory responses appear to be not corrective but helping, that is in the same direction as the core temperature deviation. A supplementary ad hoc hypothesis that setpoint level shifts explains why the thermoregulatory responses still could be considered "corrective" in spite of being in the same direction as the core temperature deviation. But supplementary ad hoc hypotheses immunize a theory to experimental challenges and therefore can no longer be considered a scientific theory. The present work shows that most of the arguments adduced to explain almost every biothermal phenomenon as being due to setpoint shifts cannot withstand a critical analysis.

Animals↗
PubMed1997

Selected temperature correlates with intensity of fever in rats.

Fever is considered due to an elevation of the setpoint of body temperature. The temperature is regulated at a higher level and the higher temperature is established by activation of the heat-seeking thermoeffectors. However, it is surprising that, for this widely accepted hypothesis, there is little experimental evidence of the setpoint shifting to a higher level. The present study shows, for the first time, a significant correlation between the magnitude of the temperature rise in fever and the ambient temperature selected by rats in a thermal gradient.

Animals↗
PubMed1996

Ethanol anapyrexia in rats.

In the present series of experiments we tested whether ethanol decreases body temperature by impairing thermal regulation (poikilothermia) or by shifting the set point downwards. The central temperature of rats kept in a thermocline and the selected ambient temperature were recorded by telemetry. After an IP injection of 2 g/kg of ethanol the rats selected an ambient temperature 7 degrees C lower than the one they selected before the ethanol injection and 8 degrees C lower than the one selected by the same rats after saline injection. At the same time the central temperature decreased by 2.5 degrees C. After about 40 min the rats preferred warmer ambient temperatures and 10 min later the central temperature began to rise. When, after ethanol, the rats were kept at 30 degrees C the central temperature remained at the normal level. At 35-36 degrees C the central temperature of normal rats without ethanol rose, in 1 h, from 37 degrees C to 39.75 degrees C. The results suggest that ethanol hypothermia is due to a downward shift of the set point and, in fact, is an anapyrexia, a condition inverse to fever.

Animals↗
PubMed1995

Emotional hyperthermia and performance in humans.

This study was carried out to see whether or not the stress induced by an academic examination raises the central temperature. A secondary object of the study was to see if examination stress might be related to the examination scores. Mean oral temperature in 108 medical students prior to examination was significantly higher than that before a laboratory demonstration. This establishes the existence of emotional hyperthermia in humans. A small but significant correlation was found between the grades obtained by the students and the difference between pre-examination and pre-demonstration temperature, higher scores being associated with larger temperature differences. However, the temperature prior to examination was practically the same in the students with the highest grades as in the students with the lowest grades. The difference between pre-examination and pre-demonstration temperature was larger in the students with the highest grades because they had a significantly lower temperature prior to the practical demonstration. On the other hand, in the lowest scoring students, temperature prior to the practical demonstration was almost as high as that prior to examination. This suggests that emotion per se does not influence the performance which apparently is related to the adequate triggering and management of the emotional response.

Adolescent↗
PubMed1992

Cold increases and warmth diminishes stress-induced rise of colonic temperature in rats.

It is generally believed that the rise of core temperature of rats induced by handling is due to a shift of set-point temperature as in fever. Changes in core temperature due to set-point shifts should not be affected by changes in the ambient temperature. Nevertheless, when the colonic temperature of rats was taken in a cold environment the usual emotional rise was higher and when the colonic temperature was taken in a warm environment the emotional rise was lower. These results contradict the hypothesis that the emotionally induced rise in temperature of rats is a fever.

Animals↗
PubMed1992

Handling elevates the colonic temperature of mice.

Handling mice for repeatedly measuring their colonic temperature (Tc) resulted in a significant rise in their Tc. When the procedure was repeated day after day, this response diminished by habituation, showing the emotional origin of Tc rise. Salicylate lowered both the maximal Tc reached during handling and the Tc before handling without affecting the difference between the initial and the maximal Tc. During the first Tc measurement in a session, concomitant to the Tc rise, ear pinna temperature decreased. When Tc reached a plateau during the last measurements, ear temperature increased. This vasomotor response suggests that stress Tc rise is a regulated Tc change. However, since, contrary to what was reported in the rat, the salicylate did not diminish the magnitude of the Tc rise, it is doubtful that the emotional Tc rise in mice is a true fever.

Affect↗
PubMed1991

Stress hyperthermia: physiological arguments that it is a fever.

The theory that stress (or emotional) rise in central temperature (Tc) in rats is a fever with an upward shift of the set-point temperature was tested with three experiments: 1) Measurement of tail skin temperature and Tc during the emotional Tc rise; 2) Investigation of the effect of ambient temperature on the emotional Tc rise; and 3) The assessment of emotional Tc rise during daytime and nighttime. Skin vasomotor responses helped the increase of Tc toward a higher level and contributed to the regulation of central temperature at this new higher level. The cold environment did not diminish the emotional rise of central temperature as it would be expected in the case of a hyperthermia. However, at night emotional fever reached a higher level than during the daytime, suggesting that prostaglandin rise in Tc is distinct from emotional or stress-induced hyperthermia. In conclusion, the experiments reported here confirm the hypothesis that the rise of Tc induced by handling or disturbance of the rats is regulated, and is due to a shift of the set-point as occurs in fever.

Animals↗
PubMed1990

Electrical hypothalamic stimulation in rats induces hyperthermia if and only if they learn to self-stimulate.

Handling and exposure to a novel environment has been shown to produce an emotional fever in rats. Electrical stimulation of lateral hypothalamus sites produced a rise of intracranial temperature not different from this emotional fever. Once the rats learned to self-stimulate, the same electrical stimulation produced a rise of the intracranial temperature significantly higher than the emotional fever. During the autoshaping for self-stimulation a significant relationship was found between the rise of the intracranial temperature and time expressed as successive days of self-stimulation training, or between the rise of intracranial temperature and the increasing frequency of operant responses. This seems to indicate that when the rats learned to self-stimulate, an initially nonsense signal, without specific thermal effect, was transformed into a neural or neurochemical code producing a new or modified effect which was a significantly higher fever.

Animals↗
PubMed1986

Circadian body temperature rhythm and behavior of rats in thermoclines.

When normal adult rats were allowed to choose among different ambient temperatures in a thermocline they selected temperatures about 224 degrees out of phase with their own intracranial temperature circadian oscillations. Without some subsidiary hypotheses, these results are difficult to reconcile with the idea that circadian body temperature rhythm is due to a cyclical shift in the set point temperature.

Animals↗
PubMed1983

Heterogeneity of hypothalamic rewarding sites possibly involved in temperature regulation.

The effect of hypothalamic self-stimulation on colonic temperature and the effect of cold and warm environments on self-stimulation rate were assessed in 97 rats. In most of the rats, self-stimulation induced a rise in colonic temperature. However, in seven animals the reverse occurred. In the whole sample self-stimulation was significantly depressed by the warm environment. The cold environment facilitated self-stimulation at some placements and inhibited it at others. From the first six placements most facilitated by the cold environment five were also most inhibited by the warm environment. When allowed to self-stimulate in the cold environment high rate self-stimulators had a significantly lower colonic temperature than when they self-stimulated at 25 degrees C while low rate self-stimulators had the same or a higher colonic temperature. Body temperature changes induced by self-stimulation on the one hand, and the effects of the cold and warm environments on self-stimulation on the other appear to be independent one from another. The results suggest that among distinct types of hypothalamic rewarding loci a few might be specifically related to temperature regulation.

Animals↗
PubMed1981

Reserpine prevents goldthioglucose hypothalamic lesions in mice.

In reserpinized mice the occurrence of goldthioglucose hypothalamic lesions was significantly lower than in control mice. Some protection was also conferred by serotonin-receptor blockers and by treatment with nialamide + DL-alpha-methyldopa, but the protective effect of reserpine was not reversed by serotonergic and dopaminergic agonists, alone or in combination, nor by insulin.

Animals↗
PubMed1979

Positive alliesthesia after insulin.

Volunteers experienced sucrose solution as more pleasant 36-48 min after insulin, than after saline control. These changes in affective estimates correlate negatively with blood sugar at 30 min and positively at 50 min after the insulin injection.

Blood Glucose↗