The hindbrain is a site of energy balance action for prolactin-releasing peptide: feeding and thermic effects from GPR10 stimulation of the nucleus tractus solitarius …

XS Davis, HJ Grill - Psychopharmacology, 2018 - Springer
Psychopharmacology, 2018Springer
Abstract Purpose Prolactin-releasing peptide (PrRP) is a neuropeptide that suppresses food
intake and increases body temperature when delivered to the forebrain ventricularly or
parenchymally. However, PrRP's receptor GPR10 is widely distributed throughout the brain
with particularly high levels found in the dorsomedial hindbrain. Thus, we hypothesized that
hindbrain-directed PrRP administration would affect energy balance and motivated feeding
behavior. Methods To address this hypothesis, a range of behavioral and physiologic …
Purpose
Prolactin-releasing peptide (PrRP) is a neuropeptide that suppresses food intake and increases body temperature when delivered to the forebrain ventricularly or parenchymally. However, PrRP’s receptor GPR10 is widely distributed throughout the brain with particularly high levels found in the dorsomedial hindbrain. Thus, we hypothesized that hindbrain-directed PrRP administration would affect energy balance and motivated feeding behavior.
Methods
To address this hypothesis, a range of behavioral and physiologic variables were measured in Sprague-Dawley rats that received PrRP delivered to the fourth ventricle (4V) or the nucleus of the solitary tract (NTS) at the level of the area postrema (AP).
Results
4V PrRP delivery decreased chow intake and body weight, in part, through decreasing meal size in ad libitum maintained rats tested at dark onset. PrRP inhibited feeding when delivered to the nucleus tractus solitarius (NTS), but not to more ventral hindbrain structures. In addition, 4V as well as direct NTS administration of PrRP increased core temperature. By contrast, 4V PrRP did not reduce ad libitum intake of highly palatable food or the motivation to work for or seek palatable foods.
Conclusions
The dorsomedial hindbrain and NTS/AP, in particular, are sites of action in PrRP/GPR10-mediated control of chow intake, core temperature, and body weight.
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