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Presynaptic dysregulation of the paraventricular thalamic nucleus causes depression-like behavior
The paraventricular thalamic nucleus (PVT) is a part of epithalamus and sends outputs to emotion-related brain areas such as the medial prefrontal cortex, nucleus accumbens, and amygdala. Various functional roles of the PVT in emotion-related behaviors are drawing attention. Here, we investigated th...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Nature Publishing Group UK
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6848207/ https://www.ncbi.nlm.nih.gov/pubmed/31712646 http://dx.doi.org/10.1038/s41598-019-52984-y |
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author | Kato, Tomoaki M. Fujimori-Tonou, Noriko Mizukami, Hiroaki Ozawa, Keiya Fujisawa, Shigeyoshi Kato, Tadafumi |
author_facet | Kato, Tomoaki M. Fujimori-Tonou, Noriko Mizukami, Hiroaki Ozawa, Keiya Fujisawa, Shigeyoshi Kato, Tadafumi |
author_sort | Kato, Tomoaki M. |
collection | PubMed |
description | The paraventricular thalamic nucleus (PVT) is a part of epithalamus and sends outputs to emotion-related brain areas such as the medial prefrontal cortex, nucleus accumbens, and amygdala. Various functional roles of the PVT in emotion-related behaviors are drawing attention. Here, we investigated the effect of manipulation of PVT neurons on the firing patterns of medial prefrontal cortical (mPFC) neurons and depression-like behavior. Extracellular single-unit recordings revealed that acute activation of PVT neurons by hM3Dq, an activation type of designer receptors exclusively activated by designer drugs (DREADDs), and administration of clozapine N-oxide (CNO) caused firing rate changes in mPFC neurons. Moreover, chronic presynaptic inhibition in PVT neurons by tetanus toxin (TeTX) increased the proportion of interneurons among firing neurons in mPFC and shortened the immobility time in the forced swimming test, whereas long-term activation of PVT neurons by hM3Dq caused recurrent hypoactivity episodes. These findings suggest that PVT neurons regulate the excitation/inhibition balance in the mPFC and mood stability. |
format | Online Article Text |
id | pubmed-6848207 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-68482072019-11-19 Presynaptic dysregulation of the paraventricular thalamic nucleus causes depression-like behavior Kato, Tomoaki M. Fujimori-Tonou, Noriko Mizukami, Hiroaki Ozawa, Keiya Fujisawa, Shigeyoshi Kato, Tadafumi Sci Rep Article The paraventricular thalamic nucleus (PVT) is a part of epithalamus and sends outputs to emotion-related brain areas such as the medial prefrontal cortex, nucleus accumbens, and amygdala. Various functional roles of the PVT in emotion-related behaviors are drawing attention. Here, we investigated the effect of manipulation of PVT neurons on the firing patterns of medial prefrontal cortical (mPFC) neurons and depression-like behavior. Extracellular single-unit recordings revealed that acute activation of PVT neurons by hM3Dq, an activation type of designer receptors exclusively activated by designer drugs (DREADDs), and administration of clozapine N-oxide (CNO) caused firing rate changes in mPFC neurons. Moreover, chronic presynaptic inhibition in PVT neurons by tetanus toxin (TeTX) increased the proportion of interneurons among firing neurons in mPFC and shortened the immobility time in the forced swimming test, whereas long-term activation of PVT neurons by hM3Dq caused recurrent hypoactivity episodes. These findings suggest that PVT neurons regulate the excitation/inhibition balance in the mPFC and mood stability. Nature Publishing Group UK 2019-11-11 /pmc/articles/PMC6848207/ /pubmed/31712646 http://dx.doi.org/10.1038/s41598-019-52984-y Text en © The Author(s) 2019 Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Kato, Tomoaki M. Fujimori-Tonou, Noriko Mizukami, Hiroaki Ozawa, Keiya Fujisawa, Shigeyoshi Kato, Tadafumi Presynaptic dysregulation of the paraventricular thalamic nucleus causes depression-like behavior |
title | Presynaptic dysregulation of the paraventricular thalamic nucleus causes depression-like behavior |
title_full | Presynaptic dysregulation of the paraventricular thalamic nucleus causes depression-like behavior |
title_fullStr | Presynaptic dysregulation of the paraventricular thalamic nucleus causes depression-like behavior |
title_full_unstemmed | Presynaptic dysregulation of the paraventricular thalamic nucleus causes depression-like behavior |
title_short | Presynaptic dysregulation of the paraventricular thalamic nucleus causes depression-like behavior |
title_sort | presynaptic dysregulation of the paraventricular thalamic nucleus causes depression-like behavior |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6848207/ https://www.ncbi.nlm.nih.gov/pubmed/31712646 http://dx.doi.org/10.1038/s41598-019-52984-y |
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