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Thermogenesis in brown adipose tissue: increase by 5-HT2A receptor activation and decrease by 5-HT1A receptor
Youichirou Ootsuka1, William W Blessing
1Department of Human Physiology, Centre for Neuroscience, School of Medicine, Flinders University, Bedford Park, SA 5042, Australia. yoichiro.otsuka@flinders.edu.au
Neuroscience Letters
|November 19, 2005
Summary
Serotonin 5-HT1A agonists decrease brown adipose tissue (BAT) thermogenesis and core body temperature, while 5-HT2A agonists increase them. These receptors modulate sympathetic outflow, affecting heat production and dissipation.
Area of Science:
- Neuroscience
- Physiology
- Pharmacology
Background:
- Body temperature regulation involves complex central and peripheral mechanisms.
- Serotonin (5-hydroxytryptamine) pathways, specifically 5-HT1A and 5-HT2A receptors, are implicated in thermoregulation.
- The role of brown adipose tissue (BAT) thermogenesis in mediating these serotonergic effects on body temperature requires further elucidation.
Purpose of the Study:
- To investigate the contribution of interscapular brown adipose tissue (iBAT) thermogenesis to body temperature changes induced by 5-HT1A and 5-HT2A receptor activation.
- To determine the influence of these serotonin receptors on sympathetic outflow to BAT and thermoregulatory cutaneous vascular beds.
Main Methods:
- Experiments were conducted in conscious, unrestrained male Sprague-Dawley rats instrumented for continuous measurement of iBAT temperature, core body temperature, and tail artery blood flow.
- Rats were exposed to thermoneutral or cold environments.
- Specific 5-HT1A (8-OH-DPAT) and 5-HT2A (DOI) agonists, along with their respective antagonists (WAY-100635 and SR 46349B), were administered subcutaneously.
Main Results:
- Activation of 5-HT1A receptors by 8-OH-DPAT decreased iBAT thermogenesis and core body temperature, an effect blocked by the 5-HT1A antagonist WAY-100635.
- Activation of 5-HT2A receptors by DOI increased iBAT thermogenesis and core body temperature, with these effects being reduced by the 5-HT2A antagonist SR 46349B.
- Both agonists modulated tail artery blood flow, indicating effects on peripheral heat dissipation.
Conclusions:
- 5-HT1A receptor activation reduces sympathetic outflow to BAT, leading to decreased heat production and core body temperature.
- 5-HT2A receptor activation increases sympathetic outflow to BAT, resulting in elevated heat production and core body temperature.
- Central serotonergic pathways involving 5-HT1A and 5-HT2A receptors coordinate BAT thermogenesis and cutaneous vascular responses to regulate body temperature.