Repeated restraint stress promotes hippocampal neuronal cell ciliogenesis and proliferation in mice
Stress severely disturbs physiological and mental homeostasis which includes adult neurogenesis in hippocampus. Neurogenesis in hippocampus is a key feature to adapt to environmental changes and highly regulated by multiple cellular signaling pathways. The primary cilium is a cellular organelle, whi...
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Published in | Laboratory animal research Vol. 34; no. 4; pp. 203 - 210 |
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Main Authors | , |
Format | Journal Article |
Language | English |
Published |
London
BioMed Central
01.12.2018
Korean Association for Laboratory Animal Science BMC 한국실험동물학회 |
Subjects | |
Online Access | Get full text |
ISSN | 1738-6055 2233-7660 |
DOI | 10.5625/lar.2018.34.4.203 |
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Summary: | Stress severely disturbs physiological and mental homeostasis which includes adult neurogenesis in hippocampus. Neurogenesis in hippocampus is a key feature to adapt to environmental changes and highly regulated by multiple cellular signaling pathways. The primary cilium is a cellular organelle, which acts as a signaling center during development and neurogenesis in adult mice. However, it is not clear how the primary cilia are involved in the process of restraint (RST) stress response. Using a mouse model, we examined the role of primary cilia in repeated and acute RST stress response. Interestingly, RST stress increased the number of ciliated cells in the adult hippocampal dentate gyrus (DG). In our RST model, cell proliferation in the DG also increased in a time-dependent manner. Moreover, the analysis of ciliated cells in the hippocampal DG with cell type markers indicated that cells that were ciliated in response to acute RST stress are neurons. Taken together, these findings suggest that RST stress response is closely associated with an increase in the number of ciliated neurons and leads to an increase in cell proliferation. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 https://synapse.koreamed.org/search.php?where=aview&id=10.5625/lar.2018.34.4.203&code=0169LAR&vmode=FULL |
ISSN: | 1738-6055 2233-7660 |
DOI: | 10.5625/lar.2018.34.4.203 |