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. Author manuscript; available in PMC: 2016 May 1.
Published in final edited form as: Brain Struct Funct. 2014 Mar 16;220(3):1511–1528. doi: 10.1007/s00429-014-0741-9

Fig. 1.

Fig. 1

Schematic demonstration of the hypothalamic regulation of appetite. Peripheral satiety hormones reach POMC and NPY/AGRP neuron groups in the arcuate nucleus (ArcN) of the hypothalamus. Activation of POMC neurons by anorexigenic hormones (e.g., leptin) stimulates the hypothalamic MC4 receptor-expressing cells (e.g., CRH neurons) inhibiting appetite, while orexigenic NPY/AGRP neurons in the arcuate nucleus and the dorsomedial hypothalamus (DHth) are inhibited. In contrast, when orexigenic satiety signals (e.g., ghrelin) activate NPY/AGRP neurons, the dorsomedial hypothalamus is stimulated and the activity of PVN neurons is attenuated. As a result food intake increases. PVN paraventricular nucleus, ME median eminence, 3rd ventr third ventricle, CRH corticotrophin-releasing hormone, MC4R melanocortin 4 receptor, NPYR NPY receptor, MCH melanine-concentrating hormone. (Modified from M. Palkovits)