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Synapsin I and Synapsin II regulate neurogenesis in the dentate gyrus of adult mice
Adult neurogenesis is emerging as an important player in brain functions and homeostasis, while impaired or altered adult neurogenesis has been associated with a number of neuropsychiatric diseases, such as depression and epilepsy. Here we investigated the possibility that synapsins (Syns) I and II,...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Impact Journals LLC
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5922353/ https://www.ncbi.nlm.nih.gov/pubmed/29721159 http://dx.doi.org/10.18632/oncotarget.24655 |
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author | Barbieri, Raffaella Contestabile, Andrea Ciardo, Maria Grazia Forte, Nicola Marte, Antonella Baldelli, Pietro Benfenati, Fabio Onofri, Franco |
author_facet | Barbieri, Raffaella Contestabile, Andrea Ciardo, Maria Grazia Forte, Nicola Marte, Antonella Baldelli, Pietro Benfenati, Fabio Onofri, Franco |
author_sort | Barbieri, Raffaella |
collection | PubMed |
description | Adult neurogenesis is emerging as an important player in brain functions and homeostasis, while impaired or altered adult neurogenesis has been associated with a number of neuropsychiatric diseases, such as depression and epilepsy. Here we investigated the possibility that synapsins (Syns) I and II, beyond their known functions in developing and mature neurons, also play a role in adult neurogenesis. We performed a systematic evaluation of the distinct stages of neurogenesis in the hippocampal dentate gyrus of Syn I and Syn II knockout (KO) mice, before (2-months-old) and after (6-months-old) the appearance of the epileptic phenotype. We found that Syns I and II play an important role in the regulation of adult neurogenesis. In juvenile mice, Syn II deletion was associated with a specific decrease in the proliferation of neuronal progenitors, whereas Syn I deletion impaired the survival of newborn neurons. These defects were reverted after the appearance of the epileptic phenotype, with Syn I KO and Syn II KO mice exhibiting significant increases in survival and proliferation, respectively. Interestingly, long-term potentiation dependent on newborn neurons was present in both juvenile Syn mutants while, at later ages, it was only preserved in Syn II KO mice that also displayed an increased expression of brain-derived neurotrophic factor. This study suggests that Syns I and II play a role in adult neurogenesis and the defects in neurogenesis associated with Syn deletion may contribute to the alterations of cognitive functions observed in Syn-deficient mice. |
format | Online Article Text |
id | pubmed-5922353 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Impact Journals LLC |
record_format | MEDLINE/PubMed |
spelling | pubmed-59223532018-05-02 Synapsin I and Synapsin II regulate neurogenesis in the dentate gyrus of adult mice Barbieri, Raffaella Contestabile, Andrea Ciardo, Maria Grazia Forte, Nicola Marte, Antonella Baldelli, Pietro Benfenati, Fabio Onofri, Franco Oncotarget Research Paper Adult neurogenesis is emerging as an important player in brain functions and homeostasis, while impaired or altered adult neurogenesis has been associated with a number of neuropsychiatric diseases, such as depression and epilepsy. Here we investigated the possibility that synapsins (Syns) I and II, beyond their known functions in developing and mature neurons, also play a role in adult neurogenesis. We performed a systematic evaluation of the distinct stages of neurogenesis in the hippocampal dentate gyrus of Syn I and Syn II knockout (KO) mice, before (2-months-old) and after (6-months-old) the appearance of the epileptic phenotype. We found that Syns I and II play an important role in the regulation of adult neurogenesis. In juvenile mice, Syn II deletion was associated with a specific decrease in the proliferation of neuronal progenitors, whereas Syn I deletion impaired the survival of newborn neurons. These defects were reverted after the appearance of the epileptic phenotype, with Syn I KO and Syn II KO mice exhibiting significant increases in survival and proliferation, respectively. Interestingly, long-term potentiation dependent on newborn neurons was present in both juvenile Syn mutants while, at later ages, it was only preserved in Syn II KO mice that also displayed an increased expression of brain-derived neurotrophic factor. This study suggests that Syns I and II play a role in adult neurogenesis and the defects in neurogenesis associated with Syn deletion may contribute to the alterations of cognitive functions observed in Syn-deficient mice. Impact Journals LLC 2018-04-10 /pmc/articles/PMC5922353/ /pubmed/29721159 http://dx.doi.org/10.18632/oncotarget.24655 Text en Copyright: © 2018 Barbieri et al. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0/) 3.0 (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Paper Barbieri, Raffaella Contestabile, Andrea Ciardo, Maria Grazia Forte, Nicola Marte, Antonella Baldelli, Pietro Benfenati, Fabio Onofri, Franco Synapsin I and Synapsin II regulate neurogenesis in the dentate gyrus of adult mice |
title | Synapsin I and Synapsin II regulate neurogenesis in the dentate gyrus of adult mice |
title_full | Synapsin I and Synapsin II regulate neurogenesis in the dentate gyrus of adult mice |
title_fullStr | Synapsin I and Synapsin II regulate neurogenesis in the dentate gyrus of adult mice |
title_full_unstemmed | Synapsin I and Synapsin II regulate neurogenesis in the dentate gyrus of adult mice |
title_short | Synapsin I and Synapsin II regulate neurogenesis in the dentate gyrus of adult mice |
title_sort | synapsin i and synapsin ii regulate neurogenesis in the dentate gyrus of adult mice |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5922353/ https://www.ncbi.nlm.nih.gov/pubmed/29721159 http://dx.doi.org/10.18632/oncotarget.24655 |
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