Glutamatergic projections from homeostatic to hedonic brain nuclei regulate intake of highly palatable food

Abstract Food intake is a complex behavior regulated by discrete brain nuclei that integrate homeostatic nutritional requirements with the hedonic properties of food. Homeostatic feeding (i.e. titration of caloric intake), is typically associated with hypothalamic brain nuclei, including the paraven...

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Autores principales:	Ashley E. Smith, Kehinde O. Ogunseye, Julia N. DeBenedictis, Joanna Peris, James M. Kasper, Jonathan D. Hommel
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2020
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/58cd59baf2604989a5e5eae9fd3f6bde
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spelling	oai:doaj.org-article:58cd59baf2604989a5e5eae9fd3f6bde2021-12-02T12:03:15ZGlutamatergic projections from homeostatic to hedonic brain nuclei regulate intake of highly palatable food10.1038/s41598-020-78897-92045-2322https://doaj.org/article/58cd59baf2604989a5e5eae9fd3f6bde2020-12-01T00:00:00Zhttps://doi.org/10.1038/s41598-020-78897-9https://doaj.org/toc/2045-2322Abstract Food intake is a complex behavior regulated by discrete brain nuclei that integrate homeostatic nutritional requirements with the hedonic properties of food. Homeostatic feeding (i.e. titration of caloric intake), is typically associated with hypothalamic brain nuclei, including the paraventricular nucleus of the hypothalamus (PVN). Hedonic feeding is driven, in part, by the reinforcing properties of highly palatable food (HPF), which is mediated by the nucleus accumbens (NAc). Dysregulation of homeostatic and hedonic brain nuclei can lead to pathological feeding behaviors, namely overconsumption of highly palatable food (HPF), that may drive obesity. Both homeostatic and hedonic mechanisms of food intake have been attributed to several brain regions, but the integration of homeostatic and hedonic signaling to drive food intake is less clear, therefore we aimed to identify the neuroanatomical, functional, and behavioral features of a novel PVN → NAc circuit. Using viral tracing techniques, we determined that PVN → NAc has origins in the parvocellular PVN, and that PVN → NAc neurons express VGLUT1, a marker of glutamatergic signaling. Next, we pharmacogenetically stimulated PVN → NAc neurons and quantified both gamma-aminobutyric acid (GABA) and glutamate release and phospho-cFos expression in the NAc and observed a robust and significant increase in extracellular glutamate and phospho-cFos expression. Finally, we pharmacogenetically stimulated PVN → NAc which decreased intake of highly palatable food, demonstrating that this glutamatergic circuitry regulates aspects of feeding.Ashley E. SmithKehinde O. OgunseyeJulia N. DeBenedictisJoanna PerisJames M. KasperJonathan D. HommelNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 10, Iss 1, Pp 1-9 (2020)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Ashley E. Smith Kehinde O. Ogunseye Julia N. DeBenedictis Joanna Peris James M. Kasper Jonathan D. Hommel Glutamatergic projections from homeostatic to hedonic brain nuclei regulate intake of highly palatable food
description	Abstract Food intake is a complex behavior regulated by discrete brain nuclei that integrate homeostatic nutritional requirements with the hedonic properties of food. Homeostatic feeding (i.e. titration of caloric intake), is typically associated with hypothalamic brain nuclei, including the paraventricular nucleus of the hypothalamus (PVN). Hedonic feeding is driven, in part, by the reinforcing properties of highly palatable food (HPF), which is mediated by the nucleus accumbens (NAc). Dysregulation of homeostatic and hedonic brain nuclei can lead to pathological feeding behaviors, namely overconsumption of highly palatable food (HPF), that may drive obesity. Both homeostatic and hedonic mechanisms of food intake have been attributed to several brain regions, but the integration of homeostatic and hedonic signaling to drive food intake is less clear, therefore we aimed to identify the neuroanatomical, functional, and behavioral features of a novel PVN → NAc circuit. Using viral tracing techniques, we determined that PVN → NAc has origins in the parvocellular PVN, and that PVN → NAc neurons express VGLUT1, a marker of glutamatergic signaling. Next, we pharmacogenetically stimulated PVN → NAc neurons and quantified both gamma-aminobutyric acid (GABA) and glutamate release and phospho-cFos expression in the NAc and observed a robust and significant increase in extracellular glutamate and phospho-cFos expression. Finally, we pharmacogenetically stimulated PVN → NAc which decreased intake of highly palatable food, demonstrating that this glutamatergic circuitry regulates aspects of feeding.
format	article
author	Ashley E. Smith Kehinde O. Ogunseye Julia N. DeBenedictis Joanna Peris James M. Kasper Jonathan D. Hommel
author_facet	Ashley E. Smith Kehinde O. Ogunseye Julia N. DeBenedictis Joanna Peris James M. Kasper Jonathan D. Hommel
author_sort	Ashley E. Smith
title	Glutamatergic projections from homeostatic to hedonic brain nuclei regulate intake of highly palatable food
title_short	Glutamatergic projections from homeostatic to hedonic brain nuclei regulate intake of highly palatable food
title_full	Glutamatergic projections from homeostatic to hedonic brain nuclei regulate intake of highly palatable food
title_fullStr	Glutamatergic projections from homeostatic to hedonic brain nuclei regulate intake of highly palatable food
title_full_unstemmed	Glutamatergic projections from homeostatic to hedonic brain nuclei regulate intake of highly palatable food
title_sort	glutamatergic projections from homeostatic to hedonic brain nuclei regulate intake of highly palatable food
publisher	Nature Portfolio
publishDate	2020
url	https://doaj.org/article/58cd59baf2604989a5e5eae9fd3f6bde
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Glutamatergic projections from homeostatic to hedonic brain nuclei regulate intake of highly palatable food

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