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Lighting up the hypothalamus: coordinated control of feeding behavior

Nature Neuroscience volume 14, pages 277–278 (2011)Cite this article

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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.

It could be argued that the hypothalamus was initially implicated in the control of food intake and obesity nearly 170 years ago with the first clinical description, by Bernhard Mohr, of hypothalamic-pituitary injury resulting in obesity1. At the turn of the twentieth century, Joseph Babinski and Alfred Frolich also reported a condition of obesity and retarded sexual development was attributed to hypothalamic-pituitary injury1. In the past century, several reports have advanced the concept that the hypothalamus is required for the regulation of energy balance1,2. Despite these seminal observations, throughout the decades contemporary methodologies have been a limiting factor in determining the physiological effects of perturbing signaling in vivo at the cellular and/or circuit level. In this issue of Nature Neuroscience, Aponte and colleagues3 use mouse optogenetics to probe neural circuits in the arcuate nucleus of the hypothalamus and find that POMC and AGRP neurons have counter-regulatory roles on the regulation of food intake.

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Figure 1: Optogenetics defines feeding behavior in the arcuate nucleus of the hypothalamus.

Marina Corral

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Authors and Affiliations

  1. Division of Hypothalamic Research, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas, USA

    Kevin W Williams & Joel K Elmquist

  2. Joel K. Elmquist is also in the Department of Pharmacology, University of Texas Southwestern Medical Center, Dallas, Texas, USA.,

    Joel K Elmquist

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  1. Kevin W Williams
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Correspondence to Kevin W Williams or Joel K Elmquist.

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Williams, K., Elmquist, J. Lighting up the hypothalamus: coordinated control of feeding behavior. Nat Neurosci 14, 277–278 (2011). https://doi.org/10.1038/nn0311-277

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