Dopaminergic neurons in the paraventricular hypothalamus extend the food consumption phase

  • Winda Ariyani
    Metabolic Signal Research Center, Institute for Molecular and Cellular Regulation, Gunma University
  • Chiharu Yoshikawa
    Metabolic Signal Research Center, Institute for Molecular and Cellular Regulation, Gunma University
  • Haruka Tsuneoka
    Metabolic Signal Research Center, Institute for Molecular and Cellular Regulation, Gunma University
  • Izuki Amano
    Department of Integrative Physiology, Gunma University Graduate School of Medicine
  • Itaru Imayoshi
    Center for Living Systems Information Science, Graduate School of Biostudies, Kyoto University
  • Hiroshi Ichinose
    School of Life Science and Technology, Institute of Science Tokyo
  • Chiho Sumi-Ichinose
    Department of Pharmacology, School of Medicine, Fujita Health University
  • Noriyuki Koibuchi
    Department of Integrative Physiology, Gunma University Graduate School of Medicine
  • Tadahiro Kitamura
    Metabolic Signal Research Center, Institute for Molecular and Cellular Regulation, Gunma University
  • Daisuke Kohno
    Metabolic Signal Research Center, Institute for Molecular and Cellular Regulation, Gunma University

書誌事項

公開日
2025-03-28
資源種別
journal article
権利情報
  • https://creativecommons.org/licenses/by-nc-nd/4.0/
DOI
  • 10.1073/pnas.2411069122
公開者
Proceedings of the National Academy of Sciences

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説明

<jats:p> Feeding behavior is controlled by various neural networks in the brain that are involved in different feeding phases: Food procurement, consumption, and termination. However, the specific neural circuits controlling the food consumption phase remain poorly understood. Here, we investigated the roles of dopaminergic neurons in the paraventricular nucleus of the hypothalamus (PVH) in the feeding behavior in mice. Our results indicated that the PVH dopaminergic neurons were critical for extending the food consumption phase and involved in the development of obesity through epigenetic mechanisms. These neurons synchronized with proopiomelanocortin neurons during consumption, were stimulated by proopiomelanocortin activation, and projected to the lateral habenula (LHb), where dopamine receptor D2 was involved in the increase in food consumption. In addition, upregulated tyrosine hydroxylase (TH) expression in PVH was associated with obesity and indispensable for obesity induction in mice lacking <jats:italic>Dnmt3a</jats:italic> . Taken together, our results highlight the roles of PVH dopaminergic neurons in promoting food consumption and obesity induction. </jats:p>

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