Alpha2-adrenergic receptor agonists prevent emotional hyperthermia.
Anna Antipov1, Mariana Brizuela1, William W Blessing1
1Centre for Neuroscience, College of Medicine and Public Health, Flinders University, Adelaide, SA, Australia.
Brain Research
|January 26, 2020
Summary
Clonidine, a drug targeting alpha2-adrenergic receptors, reduces emotional hyperthermia in rats by decreasing brown adipose tissue (BAT) thermogenesis. This study shows clonidine
Area of Science:
- Neuroscience
- Physiology
- Pharmacology
Background:
- Emotionally significant stimuli, like threats, increase body temperature (emotional hyperthermia).
- Brown adipose tissue (BAT) thermogenesis, mediated by the sympathetic nervous system, significantly contributes to this response.
- Alpha2-adrenergic agonists are known to inhibit fever and shivering.
Purpose of the Study:
- To investigate if systemic administration of clonidine, an alpha2-adrenoceptor agonist, attenuates emotional hyperthermia.
- To determine if clonidine affects BAT thermogenesis and sympathetic nerve discharge during an emotional stressor.
Main Methods:
- Conscious, unrestrained rats were exposed to an intruder rat to elicit emotional hyperthermia.
- BAT and body temperature were measured using pre-implanted thermistors.
- Rats were treated with vehicle or varying doses of clonidine; BAT sympathetic nerve discharge was also studied in anesthetized rats.
Main Results:
- Clonidine dose-dependently reduced intruder-elicited increases in BAT and body temperature.
- Clonidine abolished BAT sympathetic nerve discharges evoked by activation of the lateral habenula in anesthetized rats.
- Statistical analysis confirmed a significant dose-dependent effect of clonidine on BAT and body temperature.
Conclusions:
- Central alpha2-adrenergic receptor activation attenuates emotional hyperthermia.
- This attenuation occurs through the reduction of BAT thermogenesis.
- Clonidine's inhibitory effect on BAT thermogenesis is a key mechanism in mitigating emotional hyperthermia.
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