Abstract
BackgroundThe observations that patients with Parkinson's disease experience weight loss, while dopamine (DA) replacement therapy causes body weight gain, suggest that suppressing the DA system could stimulate energy expenditure. Peripheral administration of dopaminergic drugs decreases heat production by inhibition of brown adipose tissue (BAT) thermogenesis and by an increase in the threshold for muscular shivering. However, the exact neuroregulatory site through which DA modulates the activity of thermogenic thermoeffectors remains undefined.ResultsIn urethane/chloralose‐anesthetized, artificially‐ventilated rats, activation of type 2 or 3 dopamine receptors in the rostral raphe pallidus (rRPa) inhibits cold‐evoked BAT sympathetic activity, reduced BAT temperature and expired CO2, and produced hypotension and bradycardia. Anatomic evidence shows the co‐localization of TH and CTb immunoreactivities in neurons in the in the periventricular gray zona following injection of the retrograde tracer in the rRPa. These data indicate that this dopaminergic cell group projects to rRPa and is the likely source of the dopaminergic inhibition of BAT sympathetic activity.ConclusionOur data provide the first evidence that a DA input to the rRPa from periventricular gray zona modulates BAT thermogenesis and cardiovascular function. Modulating the dopaminergic input to rRPa could provide a novel therapeutic approach to promote fat oxidation, favor better glycaemic control, and accelerate weight loss.Support or Funding InformationNIH R01‐NS091066This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Published Version
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