Abstract
Hypothalamic pro-opiomelanocortin (POMC) neurons help regulate long-term energy stores. POMC neurons are also found in the nucleus tractus solitarius (NTS), a region regulating satiety. We show here that mouse brainstem NTS POMC neurons are activated by cholecystokinin (CCK) and feeding-induced satiety and that activation of the neuronal melanocortin-4 receptor (MC4-R) is required for CCK-induced suppression of feeding; the melanocortin system thus provides a potential substrate for integration of long-term adipostatic and short-term satiety signals.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Arcuate Nucleus of Hypothalamus / cytology
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Arcuate Nucleus of Hypothalamus / metabolism
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Down-Regulation
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Eating / physiology*
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Energy Metabolism / physiology
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Feeding Behavior / physiology
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Female
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Hypothalamus / cytology
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Hypothalamus / metabolism*
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Immunohistochemistry
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Male
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Mice
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Mice, Inbred C57BL
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Mice, Mutant Strains
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Neural Pathways / cytology
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Neural Pathways / metabolism
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Neurons / metabolism
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Pro-Opiomelanocortin / metabolism
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Proto-Oncogene Proteins c-fos / metabolism
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Rats
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Rats, Sprague-Dawley
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Receptor, Melanocortin, Type 4 / deficiency
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Receptor, Melanocortin, Type 4 / metabolism*
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Satiety Response / physiology*
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Sincalide / analogs & derivatives*
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Sincalide / physiology*
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Solitary Nucleus / cytology
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Solitary Nucleus / metabolism*
Substances
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8-sulfocholecystokinin octapeptide
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Proto-Oncogene Proteins c-fos
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Receptor, Melanocortin, Type 4
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Pro-Opiomelanocortin
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Sincalide