| First Author | D'Agostino G | Year | 2018 |
| Journal | Cell Metab | Volume | 28 |
| Issue | 4 | Pages | 619-630.e5 |
| PubMed ID | 30146485 | Mgi Jnum | J:268623 |
| Mgi Id | MGI:6270019 | Doi | 10.1016/j.cmet.2018.07.017 |
| Citation | D'Agostino G, et al. (2018) Nucleus of the Solitary Tract Serotonin 5-HT2C Receptors Modulate Food Intake. Cell Metab 28(4):619-630.e5 |
| abstractText | To meet the challenge to human health posed by obesity, a better understanding of the regulation of feeding is essential. Medications targeting 5-hydroxytryptamine (5-HT; serotonin) 2C receptors (htr2c; 5-HT2CR) improve obesity. Here we probed the functional significance of 5-HT2CRs specifically within the brainstem nucleus of the solitary tract (5-HT2CR(NTS)) in feeding behavior. Selective activation of 5-HT2CR(NTS) decreased feeding and was sufficient to mediate acute food intake reductions elicited by the 5-HT2CR agonist obesity medication lorcaserin. Similar to pro-opiomelanocortin neurons expressed within the hypothalamic arcuate nucleus (POMC(ARC)), a subset of POMC(NTS) neurons co-expressed 5-HT2CRs and were activated by 5-HT2CR agonists. Knockdown of POMC(NTS) prevented the acute appetite-suppressive effect of lorcaserin, whereas POMC(ARC) knockdown prevented the full anorectic effect. These data identify 5-HT2CR(NTS) as a sufficient subpopulation of 5-HT2CRs in reducing food intake when activated and reveal that 5-HT2CR agonist obesity medications require POMC within the NTS and ARC to reduce food intake. |
