Dopamine D2-receptors mediate hypothermia in mice: ICV and IP effects of agonists and antagonists

Nunes, J. L.; Sharif, Naj; Michel, Anton D.; Whiting, Roger L.

doi:10.1007/bf00966597

Cited by 31 publications

(14 citation statements)

References 24 publications

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“…Brain-penetrant dopamine agonists cause hypothermia via both D1-like and D2-like receptors (Carboni et al, 1986; Nunes et al, 1991), referred to hereafter as D1 and D2. Individually, a D1 antagonist (SCH23390, 2 mg/kg ip) or a D2 antagonist (sulpiride, 30 mg/kg ip) partially inhibited MTII hypothermia, while the combined inhibitors completely blocked MTII hypothermia (Figure 6A,B).…”

Section: Resultsmentioning

confidence: 99%

Biphasic Effect of Melanocortin Agonists on Metabolic Rate and Body Temperature

et al. 2014

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Summary The melanocortin system regulates metabolic homeostasis and inflammation. Melanocortin agonists have contradictorily been reported to both increase and decrease metabolic rate and body temperature. We find two distinct physiologic responses occurring at similar doses. Intraperitoneal administration of the nonselective melanocortin agonist MTII causes a melanocortin-4 receptor (Mc4r) mediated hypermetabolism/hyperthermia. This is preceded by a profound, transient hypometabolism/hypothermia that is preserved in mice lacking any one of Mc1r, Mc3r, Mc4r, or Mc5r. Three other melanocortin agonists also caused hypothermia, which is actively achieved via seeking a cool environment, vasodilation, and inhibition of brown adipose tissue thermogenesis. These results suggest that the hypometabolic/hypothermic effect of MTII is not due to a failure of thermoregulation. The hypometabolism/hypothermia was prevented by dopamine antagonists and MTII selectively activated arcuate nucleus dopaminergic neurons; these neurons may contribute to the hypometabolism/hypothermia. We propose that the hypometabolism/hypothermia is a regulated response, potentially beneficial during extreme physiologic stress.

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Section: Resultsmentioning

confidence: 99%

Biphasic Effect of Melanocortin Agonists on Metabolic Rate and Body Temperature

et al. 2014

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“…Dopamine has a well documented role in heat loss mechanisms in the preoptic anterior hypothalamus area (Hasegawa et al 2000), which is the main thermoregulatory centre in the brain (Boulant 2000). Also, drugs which augment dopamine metabolism in this area have a vasodilatory effect and cause a fall in core and brain temperature, whereas dopamine antagonists have the opposite effect (Nunes et al 1991). If the supplementary tyrosine in the present study maintained dopamine metabolism in the hypothalamus thus reducing the rate of Tcore increase, then this was not reflected by a lower body heat content and higher sweat rates and body mass losses in TYR.…”

Section: Discussionmentioning

confidence: 99%

Oral tyrosine supplementation improves exercise capacity in the heat

et al. 2011

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Increased brain dopamine availability improves prolonged exercise tolerance in the heat. It is unclear whether supplementing the amino-acid precursor of dopamine increases exercise capacity in the heat. Eight healthy male volunteers [mean age 32 ± 11 (SD) years; body mass 75.3 ± 8.1 kg; peak oxygen uptake ([Formula: see text]) 3.5 ± 0.3 L min(-1)] performed two exercise trials separated by at least 7 days in a randomised, crossover design. Subjects consumed 500 mL of a flavoured sugar-free drink (PLA), or the same drink with 150 mg kg body mass(-1) tyrosine (TYR) in a double-blind manner 1 h before cycling to exhaustion at a constant exercise intensity equivalent to 68 ± 5% [Formula: see text] in 30°C and 60% relative humidity. Pre-exercise plasma tyrosine:large neutral amino acids increased 2.9-fold in TYR (P < 0.01), while there was no change in PLA (P > 0.05). Subjects cycled longer in TYR compared to PLA (80.3 ± 19.7 min vs. 69.2 ± 14.0 min; P < 0.01). Core temperature, mean weighted skin temperature, heart rate, ratings of perceived exertion and thermal sensation were similar in TYR and PLA during exercise and at exhaustion (P > 0.05) despite longer exercise time in TYR. The results show that acute tyrosine supplementation is associated with increased endurance capacity in the heat in moderately trained subjects. The results also suggest for the first time that the availability of tyrosine, a nutritional dopamine precursor, can influence the ability to subjectively tolerate prolonged submaximal constant-load exercise in the heat.

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“…In rats or mice SCH had no effect on body temperature when administered subcutaneously or intracerboventricularly at various doses up to 0.5 mg/kg ( [7,9,33,37,38]. Faunt and Crocker [13] evaluated the effects of various doses of SCH on body temperature in male Sprague Dawley rats over a period of three hours.…”

Section: Effects Of Sch On Body Temperaturementioning

confidence: 99%

In hamsters the D1 receptor antagonist SCH23390 depresses ventilation during hypoxia

Schlenker

2008

Brain Research

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During exposure of animals to hypoxia, brain and blood dopamine levels increase stimulating dopaminergic receptors which influence the integrated ventilatory response to low oxygen. The purpose of the present study is to test the hypothesis, that in conscious hamsters, systemic antagonism of D 1 receptors would depress their breathing in air and in response to hypoxic and hypercapnic challenges. Nine male hamsters were treated with saline or 0.25 mg/kg SCH-23390 (SCH), a D 1 receptor antagonist that crosses the blood-brain barrier. Ventilation was determined using the barometric method and oxygen consumption and CO 2 production were evaluated utilizing the flowthrough method. During exposure to air, SCH decreased frequency of breathing. During exposure to hypoxia (10% oxygen in nitrogen), relative to saline, SCH-treated hamsters decreased minute ventilation by decreasing tidal volume and oxygen consumption but not CO 2 production. During exposure to hypercapnia (5% CO 2 in 95% O 2 ) frequency of breathing was decreased with SCH, but there was no significant effect on minute ventilation. Relative to saline treatment body temperature was lower in SCH treated hamsters by 0.6 degrees Celsius. These results demonstrate that in hamsters D 1 receptors can modulate control of ventilation in air and during hypoxia and hypercapnic exposures. Whether D 1 receptors located centrally or on carotid bodies modulate these effects is not clear from this study.

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Dopamine D2-receptors mediate hypothermia in mice: ICV and IP effects of agonists and antagonists

Cited by 31 publications

References 24 publications

Biphasic Effect of Melanocortin Agonists on Metabolic Rate and Body Temperature

Biphasic Effect of Melanocortin Agonists on Metabolic Rate and Body Temperature

Oral tyrosine supplementation improves exercise capacity in the heat

In hamsters the D1 receptor antagonist SCH23390 depresses ventilation during hypoxia

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