Abstract
Food intake is controlled by multiple converging signals: hormonal signals that provide information about energy homeostasis, but also hedonic and motivational aspects of food and food cues that can drive non-homeostatic or “hedonic” feeding. The ventral pallidum (VP) is a brain region implicated in the hedonic and motivational impact of food and foods cues, as well as consumption of rewards. Disinhibition of VP neurons has been shown to generate intense hyperphagia, or overconsumption. While VP gamma-Aminobutyric acidergic (GABA) neurons have been implicated in cue-elicited reward seeking and motivation, the role of these neurons in the hyperphagia resulting from VP activation remains unclear. Here, we used Designer Receptors Exclusively Activated by Designer Drugs (DREADDs) to activate VP GABA neurons in non-restricted male and female rats during chow and sucrose consumption. We found that activation of VP GABA neurons increases consumption of chow and sucrose in male rats, but not female rats. Together, these findings suggest that activation of VP GABA neurons can stimulate consumption of routine or highly palatable rewards selectively in male rats.
Significance statement The ventral pallidum has been implicated bidirectionally in consumption of both standard food and highly palatable rewards, but the specific neural subpopulations involved have not been identified. Here we chemogenetically excited GABAergic ventral pallidal neurons and tested consumption of standard chow and a sweet sucrose solution. We found that chemogenetic excitation of these neurons stimulated consumption of both rewards but did so specifically in male rats. These results suggest that GABAergic ventral pallidal neurons can drive overconsumption of foods in male rats, but not female rats, raising important questions about the role of ventral pallidum in consumption in females, who have been understudied in this domain.
Footnotes
Some viral vectors used in this study were generated by the University of Minnesota Viral Innovation Core, and some fluorescence images were taken at the University of Minnesota University Imaging Centers.
The authors report no conflict of interest.
This work was supported in part by National Institutes of Health grants R01DA053208 to JMR, F31AA031597 to KK, F31DA059436 to EAE, and P30DA048742, and a MnDRIVE Graduate Fellowship in Neuromodulation to AS.
↵*These authors contributed equally to this work.
This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license, which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.






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