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Microglia Are Dispensable for Developmental Dendrite Pruning of Mitral Cells in Mice
During early development, neurons in the brain often form excess synaptic connections. Later, they strengthen some connections while eliminating others to build functional neuronal circuits. In the olfactory bulb, a mitral cell initially extends multiple dendrites to multiple glomeruli but eventuall...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Society for Neuroscience
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10644373/ https://www.ncbi.nlm.nih.gov/pubmed/37890992 http://dx.doi.org/10.1523/ENEURO.0323-23.2023 |
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author | Niiyama, Tetsushi Fujimoto, Satoshi Imai, Takeshi |
author_facet | Niiyama, Tetsushi Fujimoto, Satoshi Imai, Takeshi |
author_sort | Niiyama, Tetsushi |
collection | PubMed |
description | During early development, neurons in the brain often form excess synaptic connections. Later, they strengthen some connections while eliminating others to build functional neuronal circuits. In the olfactory bulb, a mitral cell initially extends multiple dendrites to multiple glomeruli but eventually forms a single primary dendrite through the activity-dependent dendrite pruning process. Recent studies have reported that microglia facilitate synapse pruning during the circuit remodeling in some systems. It has remained unclear whether microglia are involved in the activity-dependent dendrite pruning in the developing brains. Here, we examined whether microglia are required for the developmental dendrite pruning of mitral cells in mice. To deplete microglia in the fetal brain, we treated mice with a colony-stimulating factor 1 receptor (CSF1R) inhibitor, PLX5622, from pregnancy. Microglia were reduced by >90% in mice treated with PLX5622. However, dendrite pruning of mitral cells was not significantly affected. Moreover, we found no significant differences in the number, density, and size of excitatory synapses formed in mitral cell dendrites. We also found no evidence for the role of microglia in the activity-dependent dendrite remodeling of layer 4 (L4) neurons in the barrel cortex. In contrast, the density of excitatory synapses (dendritic spines) in granule cells in the olfactory bulb was significantly increased in mice treated with PLX5622 at postnatal day (P) 6, suggesting a role for the regulation of dendritic spines. Our results indicate that microglia do not play a critical role in activity-dependent dendrite pruning at the neurite level during early postnatal development in mice. |
format | Online Article Text |
id | pubmed-10644373 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Society for Neuroscience |
record_format | MEDLINE/PubMed |
spelling | pubmed-106443732023-11-08 Microglia Are Dispensable for Developmental Dendrite Pruning of Mitral Cells in Mice Niiyama, Tetsushi Fujimoto, Satoshi Imai, Takeshi eNeuro Research Article: New Research During early development, neurons in the brain often form excess synaptic connections. Later, they strengthen some connections while eliminating others to build functional neuronal circuits. In the olfactory bulb, a mitral cell initially extends multiple dendrites to multiple glomeruli but eventually forms a single primary dendrite through the activity-dependent dendrite pruning process. Recent studies have reported that microglia facilitate synapse pruning during the circuit remodeling in some systems. It has remained unclear whether microglia are involved in the activity-dependent dendrite pruning in the developing brains. Here, we examined whether microglia are required for the developmental dendrite pruning of mitral cells in mice. To deplete microglia in the fetal brain, we treated mice with a colony-stimulating factor 1 receptor (CSF1R) inhibitor, PLX5622, from pregnancy. Microglia were reduced by >90% in mice treated with PLX5622. However, dendrite pruning of mitral cells was not significantly affected. Moreover, we found no significant differences in the number, density, and size of excitatory synapses formed in mitral cell dendrites. We also found no evidence for the role of microglia in the activity-dependent dendrite remodeling of layer 4 (L4) neurons in the barrel cortex. In contrast, the density of excitatory synapses (dendritic spines) in granule cells in the olfactory bulb was significantly increased in mice treated with PLX5622 at postnatal day (P) 6, suggesting a role for the regulation of dendritic spines. Our results indicate that microglia do not play a critical role in activity-dependent dendrite pruning at the neurite level during early postnatal development in mice. Society for Neuroscience 2023-11-08 /pmc/articles/PMC10644373/ /pubmed/37890992 http://dx.doi.org/10.1523/ENEURO.0323-23.2023 Text en Copyright © 2023 Niiyama et al. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license (https://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed. |
spellingShingle | Research Article: New Research Niiyama, Tetsushi Fujimoto, Satoshi Imai, Takeshi Microglia Are Dispensable for Developmental Dendrite Pruning of Mitral Cells in Mice |
title | Microglia Are Dispensable for Developmental Dendrite Pruning of Mitral Cells in Mice |
title_full | Microglia Are Dispensable for Developmental Dendrite Pruning of Mitral Cells in Mice |
title_fullStr | Microglia Are Dispensable for Developmental Dendrite Pruning of Mitral Cells in Mice |
title_full_unstemmed | Microglia Are Dispensable for Developmental Dendrite Pruning of Mitral Cells in Mice |
title_short | Microglia Are Dispensable for Developmental Dendrite Pruning of Mitral Cells in Mice |
title_sort | microglia are dispensable for developmental dendrite pruning of mitral cells in mice |
topic | Research Article: New Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10644373/ https://www.ncbi.nlm.nih.gov/pubmed/37890992 http://dx.doi.org/10.1523/ENEURO.0323-23.2023 |
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