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

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+] activati...

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Bibliographic Details
Main Authors: Chen, Naiyan, Sugihara, Hiroki, Kim, Jinah, Fu, Zhanyan, Barak, Boaz, Sur, Mriganka, Feng, Guoping, Han, Weiping
Other Authors: Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences
Format: Article
Language:en_US
Published: eLife Sciences Publications, Ltd. 2017
Online Access:http://hdl.handle.net/1721.1/109912
https://orcid.org/0000-0002-2196-8737
https://orcid.org/0000-0001-9473-2402
https://orcid.org/0000-0002-4120-4048
https://orcid.org/0000-0003-2442-5671
https://orcid.org/0000-0002-8021-277X
Description
Summary: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.