Abstract
We found that leptin receptors were expressed in hypothalamic astrocytes and that their conditional deletion led to altered glial morphology and synaptic inputs onto hypothalamic neurons involved in feeding control. Leptin-regulated feeding was diminished, whereas feeding after fasting or ghrelin administration was elevated in mice with astrocyte-specific leptin receptor deficiency. These data reveal an active role of glial cells in hypothalamic synaptic remodeling and control of feeding by leptin.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Astrocytes / physiology*
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Cell Count
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Eating / physiology*
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Excitatory Postsynaptic Potentials / physiology
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Glial Fibrillary Acidic Protein / genetics
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Glial Fibrillary Acidic Protein / metabolism
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Hypothalamus / cytology
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Hypothalamus / physiology*
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Immunohistochemistry
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In Situ Hybridization
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Leptin / genetics
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Leptin / physiology*
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Male
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Melanocortins / physiology
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Mice
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Mice, Knockout
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Microscopy, Electron
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Nerve Net / physiology*
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Neurons / physiology*
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Primary Cell Culture
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Pro-Opiomelanocortin / physiology
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Pulmonary Gas Exchange / physiology
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RNA, Messenger / biosynthesis
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RNA, Messenger / genetics
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Real-Time Polymerase Chain Reaction
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Signal Transduction / physiology*
Substances
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Glial Fibrillary Acidic Protein
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Leptin
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Melanocortins
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RNA, Messenger
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Pro-Opiomelanocortin