INTRODUCTION

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THE INDUCTION OF psychological stress in a number of species, including rats (7), mice (8), pigs (20), and humans (15, 21), is often accompanied by an elevation of core temperature commonly referred to as stress-induced hyperthermia. Methods of inciting psychological stress in the laboratory have included handling with (1, 5) or without (7, 8) accompanying intraperitoneal injection, restraint (20, 23, 26), cage switching (14), exposure to a novel environment (12, 24), exposure to noise (25), and anticipation of an aversive event (11, 28). In addition, humans have been shown to exhibit an elevation of core temperature in anticipation of sporting events (21) and before writing examinations (4, 15).

Stress-induced hyperthermia, at least in rats, is thought to result from a "regulated" thermoregulatory response since it occurs when animals are studied in both warm and cold environments (2, 6, 14) and is accompanied by activation of heat-producing (23) and heat-conserving mechanisms (5, 6). Although the mechanisms that initiate stress-induced hyperthermia are not clear, prostaglandins (5, 24) and endogenous opioids (1, 19) appear to play important roles in mediating the core temperature response, and glucocorticoids appear to play an important role in modulating (16, 18) the core temperature response. Circulating interleukin (IL)-1 does not appear to be involved in mediating stress-induced hyperthermia, as Long et al. (13) and Watkins et al. (27) have shown that neither an intraperitoneal injection of antiserum against IL-1 nor a subcutaneous injection of recombinant human IL-1 receptor antagonist alters the core temperature response of rats following exposure to a novel environment.

With regard to thermoregulatory effectors, previous experiments have focused on either autonomic thermoregulatory effectors (5, 6, 23) or on behavioral thermoregulatory effectors (3, 9) as means to increase core temperature following the induction of psychological stress. If stress-induced hyperthermia is indeed a regulated thermoregulatory response, one might expect to see a coordination of autonomic and behavioral thermoregulatory effectors in producing the core temperature response. Therefore, the aim of the present study was to investigate the thermoregulatory responses of rats when they were allowed to utilize behavioral as well as autonomic thermoregulatory effectors to alter their core temperature following exposure to psychological stress (i.e., handling followed by a sham intraperitoneal injection). Specifically, we sought to determine whether the latency, duration, magnitude, or thermoregulatory effector mechanism of the core temperature response to psychological stress would be altered when rats were given an opportunity to utilize behavioral as well as autonomic thermoregulation.

	METHODS

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Experiments were carried out on 15 female Sprague-Dawley rats (Charles River Breeding Laboratories) weighing 172 ± 7 g at the time of study. The rats were housed singly in Plexiglas cages containing Aspen-Chip Laboratory Bedding (Northeastern Products) at 22 ± 1°C in a 12:12-h light-dark cycle, with lights on from 0700 to 1900. All animals had continuous access to food (Lab Diet 5001) and tap water.

Surgical Preparation

All surgical and experimental procedures were carried out in accordance with the Guide to the Care and Use of Experimental Animals provided by the Canadian Council on Animal Care and with approval from the Animal Care Committee at the University of Calgary.

Experimental Protocol

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On the establishment of a suitable control period, the rat was removed from her cage, given a sham intraperitoneal injection (i.e., the abdominal wall was pierced with a sterile 25-gauge needle), and was placed into either a thermocline or a metabolic chamber by random assignment. Core temperature, selected ambient temperature, oxygen consumption, and behavioral observations were recorded at 6-min intervals for the duration of a 2-h experiment. Each animal was studied only once.

Experimental Apparatus

Thermocline. The thermocline used in our experiments consisted of a sealed Plexiglas cylinder (2 m long, ID 0.12 m) with a plastic grid along the bottom into which flowed room air at 2.0 l/min. A linear temperature gradient from 7 to 42°C was produced in the thermocline by circulating hot and cold water (Endocal Refrigerated Circulating Bath RTE-8DD, Neslab) into two copper coils wrapped around the cylinder.

Metabolic chamber. The metabolic chamber consisted of a double-walled Plexiglas cylinder (2 m long; ID 0.12 m) with a plastic grid along the bottom into which flowed room air at 2.0 l/min. Chamber ambient temperature was regulated at 25°C by circulating water from a temperature-controlled bath (VWR Scientific, model 1147) through the space between the walls.

Experimental Measurements and Calculations

Statistical Analysis

	RESULTS

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The rats studied in the thermocline selected a warm ambient temperature following the sham intraperitoneal injection and exhibited an increase in core temperature of shorter latency, greater magnitude, and greater duration than those studied in the metabolic chamber (Figs. 1 and 2). The rats studied in the metabolic chamber exhibited an oxygen consumption response of greater magnitude and duration than the animals studied in the thermocline (Fig. 3).

View larger version (35K): [in this window] [in a new window]   Fig. 1.   Ambient temperatures of female rats after exposure to a novel stimulus. Metabolic chamber (A), n = 8; thermocline (B), n = 7. Data are modes.

View larger version (29K): [in this window] [in a new window]   Fig. 2.   Core temperatures of female rats before (control; C) and after exposure to a novel stimulus. Metabolic chamber (A), n = 8; thermocline (B), n = 7. Data are means ± SD. * P < 0.05 vs. control by ANOVA and Newman-Keuls.

View larger version (35K): [in this window] [in a new window]   Fig. 3.   Oxygen consumption of female rats before (C) and after exposure to a novel stimulus. Metabolic chamber (A), n = 4; thermocline (B), n = 4. Data are means ± SD. * P < 0.05 vs. control by ANOVA and Newman-Keuls.

	DISCUSSION

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Our experiments provide new information about thermoregulatory effector responses of rats following exposure to a novel stimulus. Novel findings in our study were 1) rats placed in a thermocline following exposure to a novel stimulus exhibited an increase in core temperature of shorter latency, greater magnitude, and greater duration than those placed in a metabolic chamber regulated to 25°C; 2) rats placed in a thermocline following exposure to a novel stimulus selected warm and cool ambient temperatures during development of the core temperature response and during return toward control core temperature; and 3) rats placed in a metabolic chamber following exposure to a novel stimulus exhibited an oxygen consumption response of greater magnitude and duration than the animals studied in the thermocline. Thus the characteristics in addition to the effector mechanisms of the core temperature response to psychological stress are altered when rats are allowed to use behavioral in addition to autonomic thermoregulatory effectors.

Following exposure to a novel stimulus, the rats that were studied in the thermocline selected a warm ambient temperature, which facilitated a core temperature response of shorter latency, greater magnitude, and greater duration than that observed when the rats were studied in the metabolic chamber. Thus our data support the conclusions of previous studies that stress-induced hyperthermia results from a regulated rather than a "forced" thermoregulatory response. These previous studies have provided the observations that 1) vasomotor responses occur that raise and defend the increase in core temperature induced by psychological stress (5, 6), and 2) core temperature increases the same in warm and cool environments (6, 14); this latter observation has, however, been challenged (2). In our experiments, if the rise in core temperature had resulted from a forced thermoregulatory response, one would have expected the rat to select a cool region in the thermocline to accelerate heat loss, with resulting attenuation of the core temperature response compared with that observed when the rats were studied in the metabolic chamber regulated to 25°C.

The results of our experiments on selected ambient temperature in a thermocline following exposure to a novel stimulus do not agree with the those of Briese (3). He found that, although male Wistar rats exhibited an increase in core temperature following exposure to a novel stimulus, they selected a cooler ambient temperature in a thermocline. Although the reason for the apparent discrepancy between his results and ours is not clear, it may be due to the strain and/or gender of the rats used or to the magnitude of the stimulus that elicited the thermoregulatory response. Briese (3) repeatedly handled his rats and inserted a rectal probe for colonic temperature measurements every 5 min until a maximal core temperature response was obtained (e.g., ~2°C in some experiments; see Fig. 1 in Ref. 3), whereas we handled our animals once and gave one sham intraperitoneal injection, which elicited a core temperature response of ~1°C. It is possible that the greater stimulus used in his experiments forced core temperature above the increased central nervous system thermoregulatory "set point" and that this elicited a behavioral response that limited the core temperature response.

When given the opportunity to use behavioral and/or autonomic thermoregulatory effectors to raise core temperature following exposure to a novel stimulus, the rats in our study favored a behavioral response. This agrees with the previous observations that rodents preferentially utilize behavioral rather than autonomic effectors to thermoregulate during heat or cold stress (10, 17, 22). Thus, when given a choice, rats use the most energy-efficient mechanism to mount a thermoregulatory response. As far as we are aware, the neurophysiological basis of this "choice" of a more energy-efficient thermoregulatory effector is unknown.

In summary, our data show that when rats are allowed to use behavioral thermoregulation as well as autonomic thermoregulation following exposure to a novel stimulus, it not only alters the latency, magnitude, and duration of the thermoregulatory response but also the effector mechanisms used to mount the thermoregulatory response.