Direct modulation of GFAP-expressing glia in the arcuate nucleus bi-directionally regulates feeding
Name
Chen-2016-Direct modulation of GFAP-expressing.pdf
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Author(s)
Chen, Naiyan
Sugihara, Hiroki
Kim, Jinah
Fu, Zhanyan
Barak, Boaz
Sur, Mriganka
Feng, Guoping
Han, Weiping
Date Issued
October 2016
Journal
eLife
Publisher
eLife Sciences Publications, Ltd.
Citation
Chen, Naiyan, Hiroki Sugihara, Jinah Kim, Zhanyan Fu, Boaz Barak, Mriganka Sur, Guoping Feng, and Weiping Han. “Direct Modulation of GFAP-Expressing Glia in the Arcuate Nucleus Bi-Directionally Regulates Feeding.” eLife 5 (October 18, 2016).
Version
Final published version
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 Ca[superscript 2+] activation of glia in the mouse arcuate nucleus (ARC) reversibly induces increased food intake while disruption of Ca[superscript 2+] 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.
MIT Department
Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences
McGovern Institute for Brain Research at MIT
Picower Institute for Learning and Memory
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Creative Commons Attribution 4.0 International License
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DOI of Published Version
https://doi.org/10.7554/eLife.18716
