Direct modulation of GFAP-expressing glia in the arcuate nucleus bi-directionally regulates feeding

Naiyan Chen, Hiroki Sugihara, Jinah Kim, Zhanyan Fu, Boaz Barak, Mriganka Sur, Guoping Feng*, Weiping Han

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

85 Scopus citations

Abstract

Multiple hypothalamic neuronal populations that regulate energy balance have been identified. Although hypothalamic glia exist in abundance and form intimate structural connections with neurons, their roles in energy homeostasis are less known. Here we show that selective Ca2+ activation of glia in the mouse arcuate nucleus (ARC) reversibly induces increased food intake while disruption of Ca2+ signaling pathway in ARC glia reduces food intake. The specific activation of ARC glia enhances the activity of agouti-related protein/neuropeptide Y (AgRP/NPY)-expressing neurons but induces no net response in pro-opiomelanocortin (POMC)-expressing neurons. ARC glial activation non-specifically depolarizes both AgRP/NPY and POMC neurons but a strong inhibitory input to POMC neurons balances the excitation. When AgRP/NPY neurons are inactivated, ARC glial activation fails to evoke any significant changes in food intake. Collectively, these results reveal an important role of ARC glia in the regulation of energy homeostasis through its interaction with distinct neuronal subtype-specific pathways.

Original languageEnglish
Article numbere18716
JournaleLife
Volume5
Issue numberOCTOBER2016
DOIs
StatePublished - 18 Oct 2016
Externally publishedYes

Funding

FundersFunder number
Poitras Center for Affective Disorders Research
Agency for Science, Technology and Research
University of North Carolina
National Institutes of Health
Shermaine Thein
Autism Science Foundation
Simons Center for the Social Brain
Massachusetts Institute of Technology
A*STAR Biomedical Research Council
Simons Foundation
National Science Foundation1451125
National Eye InstituteR01EY007023, R01EY018648
National Institute of Neurological Disorders and StrokeU01NS090473

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