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Change of hypothalamic adult neurogenesis in mice by chronic treatment of fluoxetine

OBJECTIVE: More than half of patients with depression display eating disorders, such as bulimia nervosa and anorexia nervosa. Feeding centers are located in the hypothalamus, and hypothalamic adult neurogenesis has an important role in feeding and energy balance. Antidepressants, which can regulate...

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Autor principal: Ohira, Koji
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8848793/
https://www.ncbi.nlm.nih.gov/pubmed/35172883
http://dx.doi.org/10.1186/s13104-022-05954-z
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author Ohira, Koji
author_facet Ohira, Koji
author_sort Ohira, Koji
collection PubMed
description OBJECTIVE: More than half of patients with depression display eating disorders, such as bulimia nervosa and anorexia nervosa. Feeding centers are located in the hypothalamus, and hypothalamic adult neurogenesis has an important role in feeding and energy balance. Antidepressants, which can regulate adult neurogenesis in the hippocampus, olfactory bulb, and neocortex, are used for eating disorders, but it is unclear whether antidepressants change hypothalamic adult neurogenesis. In this study, we used immunohistological analysis to assess effects of the antidepressant fluoxetine (FLX) on hypothalamic adult neurogenesis of adult mice. RESULTS: Expressions of the proliferating cell marker, Ki67, and the neural stem cell marker, nestin, were significantly decreased in the hypothalamus by FLX. As regard to postmitotic cells, the number of the neural marker, NeuN, positive cells was significantly upregulated by FLX, but that of the astrocytic marker, S100B, positive cells was significantly reduced by FLX. The number of the oligodendrocyte marker, Olig2, positive cells was not changed by FLX. Interestingly, FLX treatment did not affect the total number of newly generated cells in the hypothalamus, comparing that in controls. These results suggest that FLX treatment influence hypothalamic adult neurogenesis and shift the balance between the numbers of neurons and astrocytes under studied conditions. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13104-022-05954-z.
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spelling pubmed-88487932022-02-18 Change of hypothalamic adult neurogenesis in mice by chronic treatment of fluoxetine Ohira, Koji BMC Res Notes Research Note OBJECTIVE: More than half of patients with depression display eating disorders, such as bulimia nervosa and anorexia nervosa. Feeding centers are located in the hypothalamus, and hypothalamic adult neurogenesis has an important role in feeding and energy balance. Antidepressants, which can regulate adult neurogenesis in the hippocampus, olfactory bulb, and neocortex, are used for eating disorders, but it is unclear whether antidepressants change hypothalamic adult neurogenesis. In this study, we used immunohistological analysis to assess effects of the antidepressant fluoxetine (FLX) on hypothalamic adult neurogenesis of adult mice. RESULTS: Expressions of the proliferating cell marker, Ki67, and the neural stem cell marker, nestin, were significantly decreased in the hypothalamus by FLX. As regard to postmitotic cells, the number of the neural marker, NeuN, positive cells was significantly upregulated by FLX, but that of the astrocytic marker, S100B, positive cells was significantly reduced by FLX. The number of the oligodendrocyte marker, Olig2, positive cells was not changed by FLX. Interestingly, FLX treatment did not affect the total number of newly generated cells in the hypothalamus, comparing that in controls. These results suggest that FLX treatment influence hypothalamic adult neurogenesis and shift the balance between the numbers of neurons and astrocytes under studied conditions. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13104-022-05954-z. BioMed Central 2022-02-16 /pmc/articles/PMC8848793/ /pubmed/35172883 http://dx.doi.org/10.1186/s13104-022-05954-z Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Research Note
Ohira, Koji
Change of hypothalamic adult neurogenesis in mice by chronic treatment of fluoxetine
title Change of hypothalamic adult neurogenesis in mice by chronic treatment of fluoxetine
title_full Change of hypothalamic adult neurogenesis in mice by chronic treatment of fluoxetine
title_fullStr Change of hypothalamic adult neurogenesis in mice by chronic treatment of fluoxetine
title_full_unstemmed Change of hypothalamic adult neurogenesis in mice by chronic treatment of fluoxetine
title_short Change of hypothalamic adult neurogenesis in mice by chronic treatment of fluoxetine
title_sort change of hypothalamic adult neurogenesis in mice by chronic treatment of fluoxetine
topic Research Note
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8848793/
https://www.ncbi.nlm.nih.gov/pubmed/35172883
http://dx.doi.org/10.1186/s13104-022-05954-z
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