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Confronting the loss of trophic support
Classic experiments with peripheral sympathetic neurons established an absolute dependence upon NGF for survival. A forgotten problem is how these neurons become resistant to deprivation of trophic factors. The question is whether and how neurons can survive in the absence of trophic support. Howeve...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10338843/ https://www.ncbi.nlm.nih.gov/pubmed/37456526 http://dx.doi.org/10.3389/fnmol.2023.1179209 |
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author | Hu, Hui-Lan Khatri, Latika Santacruz, Marilyn Church, Emily Moore, Christopher Huang, Tony T. Chao, Moses V. |
author_facet | Hu, Hui-Lan Khatri, Latika Santacruz, Marilyn Church, Emily Moore, Christopher Huang, Tony T. Chao, Moses V. |
author_sort | Hu, Hui-Lan |
collection | PubMed |
description | Classic experiments with peripheral sympathetic neurons established an absolute dependence upon NGF for survival. A forgotten problem is how these neurons become resistant to deprivation of trophic factors. The question is whether and how neurons can survive in the absence of trophic support. However, the mechanism is not understood how neurons switch their phenotype to lose their dependence on trophic factors, such as NGF and BDNF. Here, we approach the problem by considering the requirements for trophic support of peripheral sympathetic neurons and hippocampal neurons from the central nervous system. We developed cellular assays to assess trophic factor dependency for sympathetic and hippocampal neurons and identified factors that rescue neurons in the absence of trophic support. They include enhanced expression of a subunit of the NGF receptor (Neurotrophin Receptor Homolog, NRH) in sympathetic neurons and an increase of the expression of the glucocorticoid receptor in hippocampal neurons. The results are significant since levels and activity of trophic factors are responsible for many neuropsychiatric conditions. Resistance of neurons to trophic factor deprivation may be relevant to the underlying basis of longevity, as well as an important element in preventing neurodegeneration. |
format | Online Article Text |
id | pubmed-10338843 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-103388432023-07-14 Confronting the loss of trophic support Hu, Hui-Lan Khatri, Latika Santacruz, Marilyn Church, Emily Moore, Christopher Huang, Tony T. Chao, Moses V. Front Mol Neurosci Molecular Neuroscience Classic experiments with peripheral sympathetic neurons established an absolute dependence upon NGF for survival. A forgotten problem is how these neurons become resistant to deprivation of trophic factors. The question is whether and how neurons can survive in the absence of trophic support. However, the mechanism is not understood how neurons switch their phenotype to lose their dependence on trophic factors, such as NGF and BDNF. Here, we approach the problem by considering the requirements for trophic support of peripheral sympathetic neurons and hippocampal neurons from the central nervous system. We developed cellular assays to assess trophic factor dependency for sympathetic and hippocampal neurons and identified factors that rescue neurons in the absence of trophic support. They include enhanced expression of a subunit of the NGF receptor (Neurotrophin Receptor Homolog, NRH) in sympathetic neurons and an increase of the expression of the glucocorticoid receptor in hippocampal neurons. The results are significant since levels and activity of trophic factors are responsible for many neuropsychiatric conditions. Resistance of neurons to trophic factor deprivation may be relevant to the underlying basis of longevity, as well as an important element in preventing neurodegeneration. Frontiers Media S.A. 2023-06-23 /pmc/articles/PMC10338843/ /pubmed/37456526 http://dx.doi.org/10.3389/fnmol.2023.1179209 Text en Copyright © 2023 Hu, Khatri, Santacruz, Church, Moore, Huang and Chao. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Molecular Neuroscience Hu, Hui-Lan Khatri, Latika Santacruz, Marilyn Church, Emily Moore, Christopher Huang, Tony T. Chao, Moses V. Confronting the loss of trophic support |
title | Confronting the loss of trophic support |
title_full | Confronting the loss of trophic support |
title_fullStr | Confronting the loss of trophic support |
title_full_unstemmed | Confronting the loss of trophic support |
title_short | Confronting the loss of trophic support |
title_sort | confronting the loss of trophic support |
topic | Molecular Neuroscience |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10338843/ https://www.ncbi.nlm.nih.gov/pubmed/37456526 http://dx.doi.org/10.3389/fnmol.2023.1179209 |
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