Fig 1.
Control of food intake by the arcuate nucleus of the hypothalamus.
(A) Sagittal diagram of a rodent brain showing AgRP neurons (green) and POMC neurons (red) in the arcuate nucleus. Dashed vertical line shows coronal plane depicted in B. (B) Coronal diagram of a rodent brain showing AgRP neurons and POMC neurons in the arcuate nucleus adjacent to the 3V. (C) Functional signaling of the arcuate nucleus. The satiety hormone leptin stimulates POMC neurons and inhibits AgRP neurons within the arcuate nucleus. AgRP neurons are also directly stimulated by the orexigenic hormone ghrelin. POMC neurons stimulate downstream satiety neurons by releasing αMSH onto MC4R. AgRP neurons release AgRP, which antagonizes melanocortin receptors. AgRP neurons also release NPY and GABA, which inhibit downstream satiety neurons. 3V, third ventricle; αMSH, α-melanocyte stimulating hormone; AgRP, agouti-related peptide; GABA, γ-aminobutyric acid; MC4R, melanocortin 4 receptor; NPY, neuropeptide Y; POMC, pro-opiomelanocortin.
Fig 2.
Model for the role of TRPV1-like receptors on POMC neurons in appetite suppression.
Elevated core body temperature above 37°C is transduced by POMC neurons via TRPV1-like receptors, heteromers of TRPV1 and TRPV3/4. Increased activity in POMC neurons causes increased melanocortin signaling in downstream second order neurons that promote satiety. 3V, third ventricle; αMSH, α-melanocyte stimulating hormone; POMC, pro-opiomelanocortin; TRPV1, transient receptor potential vanilloid 1.