Lighting up the hypothalamus: coordinated control of feeding behavior

Abstract

A new optogenetics study finds that stimulation of pro-opiomelanocortin (POMC) and agouti-related peptide (AGRP) neurons acutely regulates feeding behavior. AGRP-induced hyperphagia is independent of melanocortin signaling.

Figure 1

Optogenetics defines feeding behavior in the arcuate nucleus of the hypothalamus. Photostimulation of arcuate POMC neurons results in the activation of melanocortin receptors on second-order neurons that ultimately results in decreased food intake. Light activation of arcuate AGRP neurons stimulates food intake independent of melanocortin signaling, supporting a lesser role of AGRP in mediating this acute hyperphagia through direct antagonism of melanocortin signaling (thin axon). Instead, these data emphasize a previously identified role for either a GABA-induced regulation of neurons in the parabrachial nucleus (PBN) and/or an NPY-induced activation of Y₁ receptors (thick axon) mediating this acute hyperphagia. MC_3/4, melanocortin receptors 3 and 4; PVN, paraventricular nucleus; Y₁R, NPY receptor.