Department of Molecular and Cell Biology, Harvard University, Cambridge, United States; Program in Neuroscience, Harvard University, Boston, United States
Department of Molecular and Cell Biology, Harvard University, Cambridge, United States
Robert Evan Johnson
Department of Molecular and Cell Biology, Harvard University, Cambridge, United States; Program in Neuroscience, Harvard University, Boston, United States
Deepak Ailani
Laboratory of Molecular and Developmental Biology, National Institute of Genetics, Department of Genetics, SOKENDAI (The Graduate University for Advanced Studies), Mishima, Japan
Owen Randlett
Department of Molecular and Cell Biology, Harvard University, Cambridge, United States
Ji-Yoon Kim
Department of Molecular and Cell Biology, Harvard University, Cambridge, United States
Maxim Nikitchenko
Department of Molecular and Cell Biology, Harvard University, Cambridge, United States
Laboratory of Molecular and Developmental Biology, National Institute of Genetics, Department of Genetics, SOKENDAI (The Graduate University for Advanced Studies), Mishima, Japan
Florian Engert
Department of Molecular and Cell Biology, Harvard University, Cambridge, United States
Medial and lateral hypothalamic loci are known to suppress and enhance appetite, respectively, but the dynamics and functional significance of their interaction have yet to be explored. Here we report that, in larval zebrafish, primarily serotonergic neurons of the ventromedial caudal hypothalamus (cH) become increasingly active during food deprivation, whereas activity in the lateral hypothalamus (LH) is reduced. Exposure to food sensory and consummatory cues reverses the activity patterns of these two nuclei, consistent with their representation of opposing internal hunger states. Baseline activity is restored as food-deprived animals return to satiety via voracious feeding. The antagonistic relationship and functional importance of cH and LH activity patterns were confirmed by targeted stimulation and ablation of cH neurons. Collectively, the data allow us to propose a model in which these hypothalamic nuclei regulate different phases of hunger and satiety and coordinate energy balance via antagonistic control of distinct behavioral outputs.
