Brs3 neurons in the mouse dorsomedial hypothalamus regulate body temperature, energy expenditure and heart rate, but not food intake
Autor: | Vojtěch Škop, Sebastian H. Zahler, Oksana Gavrilova, Ramón A. Piñol, Chia Li, Michael J. Krashes, Brandon K. Tan, Atreyi Saha, Cuiying Xiao, Marc L. Reitman |
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Jazyk: | angličtina |
Rok vydání: | 2018 |
Předmět: |
0301 basic medicine
Male endocrine system medicine.medical_specialty Dorsomedial Hypothalamic Nucleus Stimulation Optogenetics Biology Energy homeostasis Article Body Temperature 03 medical and health sciences Eating Mice Heart Rate Internal medicine Brown adipose tissue medicine Animals Neurons Raphe General Neuroscience digestive oral and skin physiology Preoptic area Receptors Bombesin 030104 developmental biology Endocrinology medicine.anatomical_structure nervous system Hypothalamus Energy Metabolism Neuroscience Nucleus |
Zdroj: | Nature neuroscience |
ISSN: | 1546-1726 1097-6256 |
Popis: | Bombesin-like receptor 3 (BRS3) is an orphan G-protein-coupled receptor that regulates energy homeostasis and heart rate. We report that acute activation of Brs3-expressing neurons in the dorsomedial hypothalamus (DMHBrs3) increased body temperature (Tb), brown adipose tissue temperature, energy expenditure, heart rate, and blood pressure, with no effect on food intake or physical activity. Conversely, activation of Brs3 neurons in the paraventricular nucleus of the hypothalamus had no effect on Tb or energy expenditure, but suppressed food intake. Inhibition of DMHBrs3 neurons decreased Tb and energy expenditure, suggesting a necessary role in Tb regulation. We found that the preoptic area provides major input (excitatory and inhibitory) to DMHBrs3 neurons. Optogenetic stimulation of DMHBrs3 projections to the raphe pallidus increased Tb. Thus, DMHBrs3→raphe pallidus neurons regulate Tb, energy expenditure, and heart rate, and Brs3 neurons in the paraventricular nucleus of the hypothalamus regulate food intake. Brs3 expression is a useful marker for delineating energy metabolism regulatory circuitry. |
Databáze: | OpenAIRE |
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