Rise In Tail Skin Temperature Research Articles

Effects of Estrogen and Keishibukuryogan on Hot Flash-like Symptoms Induced by Yohimbine in Ovariectomized Rats

Hot flash (HF) is the most common phenomenon in climacteric symptoms which often develop concomitantly with a decrease in estrogen in postmenopausal women. The onset mechanism of the hot flash is complicated and remains unclear. To date, some animal models of postmenopausal HF have been devised, but they are not fully available because of the difficulty in producing them. It is thought that hyperactivity of the central α-adrenergic system with a decrease in estrogen participates in the onset of postmenopausal HF. Therefore, in the present study, we examined whether a HF model could be easily produced by administering yohimbine (YOH), a presynaptic α₂-adrenoceptor antagonist which promotes norepinephrine release, to female rats. HF-like symptoms such as a rise in tail skin temperature and a fall in rectal temperature were shown in the rats who received YOH (3 mg/kg) subcutaneously seven days after the ovariectomy (OVX). Such symptoms following YOH administration were observed in sham rats as well, but were much more clearly noted in OVX rats. We next examined the effects of various drugs, which are clinically effective against postmenopausal HF, on HF-like symptoms in YOH-treated OVX rats: clonidine, a presynaptic α₂-adrenoceptor agonist which inhibits norepinephrine release; β-estradiol as an estrogen; and Keishibukuryogan, a Kampo medicine. These drugs inhibited HF-like symptoms in YOH-treated OVX rats. These results suggest that the activity of the α-adrenergic system is enhanced with a decrease in estrogen in OVX rats whereby YOH causes HF-like symptoms more conspicuously than in sham rats. Therefore, it is thought that YOH-treated OVX rats will be a novel and simple model of postmenopausal HF.

S-equol and the fermented soy product SE5-OH containing S-equol similarly decrease ovariectomy-induced increase in rat tail skin temperature in an animal model of hot flushes

The aim of this study was to compare the effect of SE5-OH, a fermented soy product containing S-equol, with purified S-equol on hot flushes in an ovariectomized rat model. Eleven-week-old female Sprague-Dawley rats were assigned to either the sham group (vehicle; n = 30) or one of four ovariectomized groups: control (vehicle; n = 30), conjugated equine estrogens (CEE; 6.0 mg kg(-1) d(-1) CEE; n = 10), SE5-OH (2,000 mg kg(-1) d(-1) SE5-OH containing 11.7 mg kg(-1) d(-1) as S-equol; n = 30), and S-equol (11.7 mg kg(-1) d(_1) S-equol; n = 30). Three days after sham operation or ovariectomy, animals were treated once daily for 38 days. Tail skin temperature (TST) was assessed on days 21, 28, and 35 after surgery. Plasma estradiol and follicle-stimulating hormone levels and uterine weight and uteri histology were evaluated at the end of treatment. The rise in TST resulting from ovariectomy was inhibited by CEE, SE5-OH, and S-equol. Compared with the control, TST was decreased by 68.9% and 86.2% in SE5-OH group on days 21 and 28, respectively (P = 0.014, 0.020), and by 60.1% and 89.1% in S-equol group, respectively (P = 0.038, 0.016). Unlike in the CEE group, plasma estradiol and follicle-stimulating hormone levels, uterine weight, epithelial height, stromal expansion, and myometrial thickness were not affected in SE5-OH and S-equol groups. The results of this animal model of hot flushes suggest that S-equol is one of the primary components of SE5-OH and that both SE5-OH and S-equol represent promising alternatives for the treatment of menopausal symptoms. Clinical research is needed to confirm these findings.

Alleviation of Thermoregulatory Dysfunction with the New Serotonin and Norepinephrine Reuptake Inhibitor Desvenlafaxine Succinate in Ovariectomized Rodent Models

Hot flushes and night sweats, referred to as vasomotor symptoms (VMS), are presumed to be a result of declining hormone levels and are the principal menopausal symptoms for which women seek medical treatment. To date, estrogens and/or some progestins are the most effective therapeutics for alleviating VMS; however, these therapies may not be appropriate for all women. Therefore, nonhormonal therapies are being evaluated. The present study investigated a new reuptake inhibitor, desvenlafaxine succinate (DVS), in animal models of temperature dysfunction. Both models used are based on measuring changes in tail-skin temperature (TST) in ovariectomized (OVX) rats. The first relies on naloxone-induced withdrawal in morphine-dependent (MD) OVX rats, resulting in an acute rise in TST. The second depends on an OVX-induced loss of TST decreases during the dark phase as measured by telemetry. An initial evaluation demonstrated abatement of the rise in TST with long-term administration of ethinyl estradiol or with a single oral dose of DVS (130 mg/kg) in the MD model. Further evaluation showed that orally administered DVS acutely and dose dependently (10-100 mg/kg) abated a naloxone-induced rise in TST of MD rats and alleviated OVX-induced temperature dysfunction in the telemetry model. Oral administration of DVS to OVX rats caused significant increases in serotonin and norepinephrine levels in the preoptic area of the hypothalamus, a key region of the brain involved in temperature regulation. These preclinical studies provide evidence that DVS directly impacts thermoregulatory dysfunction in OVX rats and may have utility in alleviating VMS associated with menopause.

Effect of OS-0689, a novel SERM, on periarterial nerve function in tail arteries of ovariectomized rats

Objective: We have previously shown that OS-0689 attenuates the rise in tail skin temperature of ovariectomized rats, which is believed to be relevant to human symptoms of hot flush. In this study, we elucidate the mechanism underlying the ameliorating effects of OS-0689 on elevated tail skin temperature. Methods: Female Sprague–Dawley rats were ovariectomized and orally treated with OS-0544 (1 mg/kg), OS-0689 (3 mg/kg; (+)-enantiomer of OS-0544) or 17β-estradiol (3 mg/kg; E 2) for 1 week. At 1, 3 or 6 weeks after ovariectomy, the vasoconstrictions and vasorelaxations induced by periarterial nerve stimulation (PNS), l-noradrenaline (NA), and rat calcitonin gene-related peptide (CGRP) in isolated tail arteries were compared between OVX and sham-operated rats. Results: Three weeks after ovariectomy, vasoconstrictions in response to PNS and NA in the arteries of OVX rats were markedly less than those in the arteries of sham-operated rats. However, at 1 and 6 weeks after ovariectomy the stimuli-induced vasoconstrictions in the arteries of OVX rats were greater than those of sham-operated rats. Moreover, NA reactivity was not attenuated in the mesenteric arteries at 3 weeks after ovariectomy. OS-0544, OS-0689 and E 2 prevented the decrease in vasoconstrictions in the tail arteries. Vasorelaxations in response to PNS and rat CGRP were significantly greater in the arteries of OVX rats than in those of the sham-operated rats. OS-0689 inhibited the increase in vasorelaxation induced by both stimuli, whereas E 2 had no effects. Conclusions: Ovariectomy not only decreases adrenergic function but also enhances CGRPergic function in rats’ tail arteries. OS-0689 improves both impairments and thereby improves on rat hot flush.

Role of angiotensin II and the subfornical organ in the pharmacological actions of ethanol.

The current study was designed to evaluate if angiotensin II mediates the hypothermic effects of ethanol, and to determine if the effects of angiotensin are mediated centrally. We also tested the hypothesis that the subfornical organ (SFO) is a site responsible for the alterations in body temperature and aerial righting reflex mediated by ethanol and for the modulation of ethanol consumption in rats. Male Sprague-Dawley rats were used in a series of experiments to evaluate the role of both peripheral and central administration of losartan, a selective angiotensin type 1 receptor antagonist on ethanol-induced hypothermia. Subsequent studies were undertaken in SFO-lesioned rats to evaluate the effects of SFO-lesion on alcohol intake, the thermal response to alcohol and angiotensin, and the aerial righting reflex. Selective antagonism of the angiotensin II type 1 receptor, administered either peripherally or centrally, attenuated not only the fall in colonic temperature but also attenuated the transient rise in tail skin temperature that was associated with administration of ethanol. The thermal responses to both angiotensin and ethanol were similarly attenuated in SFO-lesioned rats. Likewise the aerial righting reflex, which has previously been shown to be impaired by losartan treatment, was also significantly attenuated in SFO-lesioned animals. Alcohol intake, as determined by a 48 h, two-bottle preference test also revealed that SFO-lesioned animals consumed significantly less alcohol (ethanolic beer) than did controls. Collectively, the results demonstrate that ethanol-induced temperature responses are mediated by the renin-angiotensin system and that this interaction is mediated centrally. In addition, the results demonstrate that the SFO is a site that mediates several neurobiological effects of ethanol, possibly via the renin-angiotensin system.

Effects of Insulin and Acarbose Alone and in Combination in the Female Streptozotocin-lnduced Diabetic Rat

Diabetes is characterized by hyperphagia, polydipsia, polyuria, elevations in blood and urinary glucose, and alterations in the adrenergic nervous system. Insulin treatment is effective in reversing most of the adverse conditions of diabetes in the streptozotocin-treated rat. Acarbose (BAY G 5421), an intestinal alpha-glucosidase inhibitor, decreases postprandial glycemia by delaying carbohydrate absorption and also affords some beneficial effects in the diabetic animal. The purpose of this study was to evaluate the effects of chronic insulin (< or = 2 U/day) with and without acarbose treatment (20 mg/100 g of diet) on the metabolic and adrenergic parameters altered in streptozotocin (50 mg/kg, intravenously)-induced diabetes in female rats. Insulin dosage was changed weekly after the first 2 weeks of treatment in both insulin-treated groups in an attempt to maintain a level of blood glucose that was comparable to that achieved with acarbose treatment alone. Insulin dosage was reduced to a greater extent in the dual-treated group than in the group treated with insulin alone. Diabetic rats were hyperphagic, polydipsic, and polyuric within 1 week of streptozotocin treatment. Each treatment alone was effective in reducing these alterations. However, these reductions were more apparent in the combined therapy group. Only in this combined therapy group was glycated hemoglobin returned to normal. All treatments also prevented the significant weight loss observed in untreated diabetic animals. Adrenergic responses were assessed by monitoring the rise in tail skin temperature associated with administration of isoproterenol. Diabetic rats were less responsive than controls, and each of the treatments restored this response.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of the adrenal gland in the thermal response to morphine withdrawal in rats.

Administration of naloxone to morphine-dependent rats results in an elevation of tail skin temperature and a fall in core temperature. Previous studies have demonstrated a role of the adrenal gland in the thermal responses that accompany morphine withdrawal in the rat. In the present study, experiments were designed to determine if the duration of adrenalectomy significantly influenced the thermal response observed in morphine withdrawal. In addition we evaluated the influence of the adrenal medulla and glucocorticoid replacement in adrenalectomized rats in mediating the thermal responses of the morphine-dependent rat. Ovariectomized rats were addicted to morphine and subsequently withdrawn by administration of naloxone. This treatment results in a significant rise in tail skin temperature and subsequent fall in colonic temperature. These thermal responses were not observed in morphine-naive rats. Adrenalectomy resulted in a significant attenuation of the rise in tail skin temperature associated with withdrawal. This reduced tail skin temperature response was not different among animals adrenalectomized for 1, 7, 14, 21, or 28 days. Likewise, the moderate increase in core temperature associated with morphine treatment was not observed in the adrenalectomized rats. Serum corticosteroid determinations confirmed the loss of the adrenal steroids in the adrenalectomized rats. In a subsequent experiment it was determined that adrenal demedullation did not reduce the tail skin temperature response during morphine withdrawal, and corticosteroids restored the naloxone-induced surge in tail skin temperature in morphine-dependent, adrenalectomized rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of a brain-enhanced estrogen delivery system on tail-skin temperature of the rat: implications for menopausal hot flush

The menopause results from the decreasing production of ovarian estrogens/progestins. This loss of ovarian hormones in 75–85% of women leads to a number of brain-mediated steroid-withdrawal symptoms, the most frequent being hot flushes. Thus, replacement therapy with a brain-enhanced estrogen delivery system (E 2-CDS) with sustained release of estradiol (E 2) in the brain may be more effective in the treatment of menopausal symptoms than currently used estrogens. The present study was designed to evaluate the effects of E 2-CDS vs. E 2, on the tail-skin temperature (TST) surge associated with administration of naloxone to morphine-dependent rats, an animal model for menopausal hot flush. Ovariectomizcd rats received a single or multiple doses of E 2-CDS at 1.0 mg/kg body weight or E 2, (0.5 mg pellet) weekly for 1 or 3 weeks before temperature recording. The mean maximal elevation in TST of the control animals was 6.4 ± 0.2 °C. A single injection of E 2-CDS attenuated the naloxone-induced rise in TST by 25%, while multiple injections resulted in significant attenuation of the rise in TST (3.4 ± 0.6). By contrast, multiple implants of E 2 pellet (3 pellets over 3 weeks) did not affect the surge of TST. Plasma E 2 levels in animals treated with E 2-CDS were slightly increased to 13 pg/ml for single-injected and to 44 pg/ml for multiple-injected rats. However, the E 2-pellet treatment produced plasma E 2 levels that were 2-fold greater than the E 2 levels produced by multiple injections of E 2-CDS. Plasma gonadotropins (LH and FSH) were significantly suppressed with the E 2-pellet as well as the single and multiple E 2-CDS treatment. Plasma prolactin levels were significantly elevated by E 2 pellet and multiple injections of E 2-CDS. The kinetic profiles of E 2-CDS metabolites in plasma indicated an apparent t 1 2 = 8 h for E 2-Q + and 3 h for E 2. Collectively, these data support the view that E 2-CDS may be potentially useful in the treatment of vasomotor hot flushes.

Effects of acute central LH-RH administration of the skin temperature response in morphine dependent rats

There are numerous reports of a temporal relationship between LH secretion and a subsequent flushing response in menopausal women. We have developed a morphine-dependent animal model to study the mechanisms of the hot flush. Administration of naloxone to these animals results in a surge in LH secretion which precedes the elevation in tail skin temperature (TST). In the present study, we utilized central administration of an LH-RH agonist and antagonist to evaluate the skin temperature response in our animal model. Ovariectomized female rats were fitted with unilateral cannula in the lateral ventricle (LV). One week later these animals were mildly restrained to allow for continuous measurement of tail skin temperatures (TST). Central administration of naloxone was without effect in controls but produced a 5–6 °C rise of TST in the morphine-dependent rat while central administration of 10 μl of the saline vehicle produced no changes in TST in either group. A similar increased sensitivity to LH-RH was observed in morphine-dependent rats. Administration of 5 or 10 μg of the LH-RH agonist (Des-Gly 10,[im-Bzl- d-His 6]LH-RH ethylamide) into the LV produced a significantly greater elevation in TST (4 °C) in the morphine-dependent rats compared to a negligible rise in TST in the control rats; however, administration of a larger dose of 20 μg of the LH-RH agonist produced similar TST responses of about 4 °C in both groups. Intravenous administration of the LH-RH agonist (10 μg) was ineffective in producing any temperature effect in morphine-dependent rats. Thus, it appears that the morphine-dependent rat is more sensitive to the LH-RH agonist and the temperature response is mediated by a central mechanism which is similar to that observed following administration of a dose of naloxone. In a subsequent study central administration of the LH-RH agonist (5 μg/10 μl) resulted in a similar rise in serum LH in both control and morphine-dependent rats, suggesting that the elevation in TST is not closely associated with LH secretion. Further support for a role of LH-RH in our animal model was obtained following central administration of an LH-RH antagonist ([ d-Phe 2,6, Pro 3]LH-RH) which blocked the rise in TST associated with systemic administration of naloxone (1 mg/kg, s.c.) in morphine-dependent rats. Collectively, these data indicate that activation of central LH-RH receptors may initiate the temperature response observed during the hot flush and further support the hypothesis that activation of the LH-RH neuron may be involved in the pathogenesis of the hot flush syndrome.

Effects of estrus cycle on thermoregulatory responses during exercise in rats

In female rats, rectal temperature (Tre), tail vasomotor response, oxygen uptake (VO2), and carbon dioxide production (VCO2) were measured in proestrus and estrus stages during treadmill running at two different speeds at an ambient temperature (Ta) of 24 degrees C. Experiments were performed at 2.00-6.00 a.m., when the difference in Tre was greatest between the two stages; Tre at rest in the estrus stage was 0.54 degrees C higher than in the proestrus stage. In a mild warm environment, threshold Tre for a rise in tail skin temperature (Ttail) was also higher in the estrus stage than in the proestrus stage. In contrast, no difference was seen in the threshold Tre and steady state Tre at the end of exercise between proestrus and estrus stages. These values were higher at the higher work intensity. VO2 was also similar between the two stages, except in the second 5 min after the beginning of exercise, when VO2 was greater and Tre rose more steeply in the proestrus stage. These data indicate that deep body temperature during exercise is regulated at a certain level depending on the work intensity and is not influenced by the estrus cycle.

Altered tail-skin temperature responsiveness in streptozotocin-induced diabetic rats

We evaluated the tail-skin temperature response to administration of several doses of isoproterenol in streptozotocin-induced diabetic rats after 48 h and after 4 weeks of diabetes. Blood glucose concentrations were significantly increased over controls 48 hours after administration of streptozotocin (65 mg/kg, i.v.) and remained elevated to a similar degree in the 4-week group. Basal rectal temperature and tail-skin temperature (TST) were not different between controls and the diabetic groups and were not affected by administration of saline. However, administration of isoproterenol (25 μg/kg, s.c.) caused a significant rise in TST in the control group, but not in the rats diabetic for 4 weeks. A similar but exaggerated response was observed in the controls after subcutaneous administration of 40 μg/kg and 100 μg/kg of isoproterenol. The TST response in the 4-week diabetic rats still remained negligible with the two higher doses of isoproterenol. When the data were summarized as area under the TST curve, a dose-dependent increase was observed in the control groups and a significant absence of response was observed in the 4-week group. The rats studied 48 h after streptozotocin injection had a similar TST response to the control group after administration of 40 μg/kg of isoproterenol. Colonic temperatures did not significantly change between the two groups in any of the studies, although the colonic temperatures tended to rise in the control groups following administration of isoproterenol. We conclude from this study that the absence of a tail-skin temperature response in rats diabetic for 4 weeks results from either a reduced β-adrenergic receptor mediated response or an altered neural thermoregulatory reflex response, or both. These changes are probably not due to streptozotocin treatment or increases in blood glucose.

Effect of chronic estrogen on the skin temperature response to naloxone in morphine-dependent rats.

It is well documented that opioids and sex steroids modify body temperature in the rat. We have previously reported that the temperature responses to naloxone in the morphine-dependent rat was more pronounced in the female than in the male rat. In addition, ovariectomy but not castration resulted in altered temperature responses in the morphine-dependent rat, which suggests a role for estrogen in modifying the temperature responses. This study was designed to evaluate the effect of sex steroid hormones on the surge in tail skin temperature associated with administration of naloxone to morphine-dependent female rats. Ovariectomized female rats were treated with estrogen (0.5 mg pellet), progesterone (5 mg pellet), or the combined therapy for 21 days. Administration of naloxone to these morphine-dependent rats resulted in a 5.9 +/- 0.5 degrees C rise in tail skin temperature in the placebo control rats and 5.7 +/- 0.5 degrees C in the progesterone-treated group; there was a significantly reduced elevated in tail skin temperature of 3.1 +/- 1.0 degrees C and 2.9 +/- 1.0 degrees C in the and estrogen-progesterone treated groups. Body weights also were significantly depressed in the estrogen-treated groups. In a subsequent study, the effects of several doses of chronic estrogen treatment were evaluated (0.1-50 mg pellets). The elevation of tail skin temperature in response to administration of naloxone to morphine-dependent rats was significantly reduced at all doses of estrogen when compared with placebo-treated controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of opiod antagonists and their quaternary analogs on temperature changes in morphine-dependent rats

Subcutaneous administration of three opioid antagonists; naloxone, naltrexone and nalmefene, produced a significant rise in tail skin temperature and a subsequent fall in rectal temperature in morphine dependent rats. However, subcutaneous administration of equimolar concentrations of the quaternary derivatives of these opioid antagonists (naloxone methobromide, naltrexone methobromide and n-methylnalmefenium iodide) failed to produce any significant alterations in either tail skin or rectal temperatures in the morphine dependent rat. At doses of naloxone methobromide 6 to 9 times greater than naloxone, there was a slight reduction of rectal temperatures with no significant elevation of skin temperature However, the fall in reactal temperature was still significantly less than that achieved with administration of naloxone. When each of these six agents were administered centrally (20 ug/5 ul, icv) in the morphine dependent rat, similar increases in tail skin temperature and decreases in rectal temperature were observed. These temperature changes were similar to those observed following systematic administration of the opioid antagonist. Previously, we have suggested that acute withdrawal in the morphine-dependent rat may serve as an animal model for the mechanism of the menopausal hot flush. Collectively, these results suggest that the temperature changes associated with morphine-withdrawal in our rat model for studying the mechanisms of the menopausal hot flush are centrally mediated.

Regional skin temperature changes in a rat model for the menopausal hot flush

Administration of naloxone to morphine-dependent male and female rats produced a significant rise in both tail skin temperature and foot temperature with a subsequent fall in colonic temperature. The magnitudes of the skin temperature surges were similar in the two regions, with the elevation in foot temperature preceding the rise in tail skin temperature. These regional skin temperature surges were similar in magnitude, duration and temporal pattern in both the male and female rat, and are similar to those exhibited in men and women undergoing flushing episodes. Castration of males did not alter these temperature responses. The only difference in response between male and female rats was the more pronounced fall in colonic temperature observed in morphine-dependent female rats following administration of naloxone. Neither the administration of naloxone to placebo-treated animals nor that of saline to morphine-dependent animals produced any changes in skin or colonic temperature in either male or female rats. These results suggest that the pattern of skin temperature alterations associated with morphine withdrawal in both the male and female rat is similar to the pattern of skin temperature surges associated with the hot flush in men and women, which provides additional evidence for the morphine-dependent rat as a model for women who exhibit flushing episodes. Additionally, this is the first report of a potential model for men who exhibit flushing episodes.

Dopamine receptors in the central thermoregulatory pathways of the rat.

1. Intrahypothalamic injection of either dopamine (10 microgram) or apomorphine (10 microgram) in a dose volume of 1 microliter. caused an almost immediate rise in tail skin temperature and a concomitant fall in core temperature in the conscious rat maintained at an ambient temperature of 17 +/- 1 degrees C. 2. The location of the dopamine-sensitive site was defined more accurately by reducing the dose volume to 0.5 microliter. and injecting dopamine at different points throughout the preoptic and anterior hypothalamic region. 3. The largest mean fall in core temperature (1.13 +/- 0.22 degrees C) was obtained after injection into the preoptic region. Injections with their perimeters more than 0.4 mm rostral or caudal to this site were ineffective. 4. Rats placed 0.65 m below a 250 W infra-red lamp responded to the imposed heat load by vasodilation of the tail skin blood vessels, indicated by an increased tail skin temperature. 5. Bilateral, but not unilateral, injection of either pimozide (0.5 microgram) or haloperidol (2.5 microgram) into the preoptic region significantly reduced the increase in tail skin temperature so that the rats were less able to withstand the imposed heat load. 6. Three serial sections (0.5 mm thick) were prepared from the preoptic anterior hypothalamic region of the rat brain, one anterior, one posterior and one corresponding to the dopamine-sensitive site. 7. Tissue from the middle slice increased its rate of synthesis of 3,5-cyclic AMP in response to addition of dopamine 20 or 100 micron to the incubation medium. The posterior slice was inactive, but the anterior slice had similar activity to the middle slice. 8. The effect of dopamine on the middle slice was specifically blocked by haloperidol (0.1 micron), whereas the effects on the anterior slice were partially blocked by both haloperidol (0.1 micron) and propranolol (0.1 micron). 9. These results indicate that there is within a well defined area of the preoptic region a population of dopamine receptors, which play a part in the transmission of information from warm sensors to heat loss effectors.

Do central dopamine receptors have a physiological role in thermoregulation?

1 Core and tail skin temperature was measured in rats which had guide cannulae implanted into their brains to allow drug injections directly into the preoptic anterior hypothalamus. 2 Apomorphine and dopamine (10 microgram in 1 microliter) injected into the area of the preoptic anterior hypothalamus caused a fall in core temperature which was preceded by a rise in tail skin temperature. 3 The decrease in core temperature following central injection of either apomorphine or dopamine was significantly reduced by pretreating rats for 2 h with pikozide 0.5 mg/kg i.p.). 4 Bilateral intrahypothalamic injection of pimozide (0.5 microgram in 1 microliter) significantly reduced the hypothermic effect of systemic apomorphine (1.25 mg/kg i.p.). 5 Control rats placed 65 cm below a 250 W infrared lamp responded with vasodilation of tail skin blood vessels as indicated by an increase in tail skin temperature. Pimozide pretreatment (0.5 mg/kg i.p.) significantly reduced this response. 6 These results suggest that the preoptic anterior hypothalamus contains dopamine receptors which mediate hypothermia in rodents and raise the possibility that endogenous dopamine has a physiological role in thermoregulation.