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Коэкспрессия глутаматергических генов и генов аутистического спектра в гиппокампе у самцов мышей с нарушением социального поведения
There is a hypothesis of the involvement of the glutamatergic system in the development of autism. It has been shown that the chronic experience in daily intermale confrontations leads to disturbances in social behavior: a decrease in communicativeness, disturbances of socialization, emergence of st...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Federal Research Center Institute of Cytology and Genetics of Siberian Branch of the Russian Academy of Sciences
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7716547/ https://www.ncbi.nlm.nih.gov/pubmed/33659799 http://dx.doi.org/10.18699/VJ20.42-o |
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author | Коваленко, И.Л. Галямина, А.Г. Смагин, Д.А. Кудрявцева, Н.Н. |
author_facet | Коваленко, И.Л. Галямина, А.Г. Смагин, Д.А. Кудрявцева, Н.Н. |
author_sort | Коваленко, И.Л. |
collection | PubMed |
description | There is a hypothesis of the involvement of the glutamatergic system in the development of autism. It has been shown that the chronic experience in daily intermale confrontations leads to disturbances in social behavior: a decrease in communicativeness, disturbances of socialization, emergence of stereotypical behaviors that can be considered as symptoms of the autistic spectrum disorders. So, the aim of this study was to investigate changes in the expression of glutamatergic (GG) and autism-related (GA) genes in the hippocampus of animals with impaired social behavior caused by repeated experience of social defeat or aggression in daily agonistic confrontations. To form groups of animals with contrasting behaviors, a model of sensory contact (chronic social stress) was used. The collected brain samples were sequenced at JSC Genoanalytica (http://genoanalytica.ru/ , Moscow, Russia). Transcriptomic analysis revealed a down-regulation of autism-related (Shank3, Auts2, Ctnnd2, Nrxn2) and glutamatergic (Grm4) genes in aggressive mice. At the same time, the expression of GA-related genes (Shank2, Nlgn2, Ptcdh10, Reln, Arx) and GG genes (Grik3, Grm2, Grm4, Slc17a7, Slc1a4, Slc25a22) excluding Grin2a was increased in defeated mice. Correlative analysis revealed a statistically significant association between GG and GA expression. These results can serve as a confirmation of the participation of the glutamatergic system in the pathophysiology of the autistic spectrum disorder |
format | Online Article Text |
id | pubmed-7716547 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | The Federal Research Center Institute of Cytology and Genetics of Siberian Branch of the Russian Academy of Sciences |
record_format | MEDLINE/PubMed |
spelling | pubmed-77165472021-03-02 Коэкспрессия глутаматергических генов и генов аутистического спектра в гиппокампе у самцов мышей с нарушением социального поведения Коваленко, И.Л. Галямина, А.Г. Смагин, Д.А. Кудрявцева, Н.Н. Vavilovskii Zhurnal Genet Selektsii Review There is a hypothesis of the involvement of the glutamatergic system in the development of autism. It has been shown that the chronic experience in daily intermale confrontations leads to disturbances in social behavior: a decrease in communicativeness, disturbances of socialization, emergence of stereotypical behaviors that can be considered as symptoms of the autistic spectrum disorders. So, the aim of this study was to investigate changes in the expression of glutamatergic (GG) and autism-related (GA) genes in the hippocampus of animals with impaired social behavior caused by repeated experience of social defeat or aggression in daily agonistic confrontations. To form groups of animals with contrasting behaviors, a model of sensory contact (chronic social stress) was used. The collected brain samples were sequenced at JSC Genoanalytica (http://genoanalytica.ru/ , Moscow, Russia). Transcriptomic analysis revealed a down-regulation of autism-related (Shank3, Auts2, Ctnnd2, Nrxn2) and glutamatergic (Grm4) genes in aggressive mice. At the same time, the expression of GA-related genes (Shank2, Nlgn2, Ptcdh10, Reln, Arx) and GG genes (Grik3, Grm2, Grm4, Slc17a7, Slc1a4, Slc25a22) excluding Grin2a was increased in defeated mice. Correlative analysis revealed a statistically significant association between GG and GA expression. These results can serve as a confirmation of the participation of the glutamatergic system in the pathophysiology of the autistic spectrum disorder The Federal Research Center Institute of Cytology and Genetics of Siberian Branch of the Russian Academy of Sciences 2020-03 /pmc/articles/PMC7716547/ /pubmed/33659799 http://dx.doi.org/10.18699/VJ20.42-o Text en Copyright © AUTHORS, 2020 https://creativecommons.org/licenses/by/2.5/This work is licensed under a Creative Commons Attribution 4.0 License |
spellingShingle | Review Коваленко, И.Л. Галямина, А.Г. Смагин, Д.А. Кудрявцева, Н.Н. Коэкспрессия глутаматергических генов и генов аутистического спектра в гиппокампе у самцов мышей с нарушением социального поведения |
title | Коэкспрессия глутаматергических генов
и генов аутистического спектра в гиппокампе
у самцов мышей с нарушением социального поведения |
title_full | Коэкспрессия глутаматергических генов
и генов аутистического спектра в гиппокампе
у самцов мышей с нарушением социального поведения |
title_fullStr | Коэкспрессия глутаматергических генов
и генов аутистического спектра в гиппокампе
у самцов мышей с нарушением социального поведения |
title_full_unstemmed | Коэкспрессия глутаматергических генов
и генов аутистического спектра в гиппокампе
у самцов мышей с нарушением социального поведения |
title_short | Коэкспрессия глутаматергических генов
и генов аутистического спектра в гиппокампе
у самцов мышей с нарушением социального поведения |
title_sort | коэкспрессия глутаматергических генов
и генов аутистического спектра в гиппокампе
у самцов мышей с нарушением социального поведения |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7716547/ https://www.ncbi.nlm.nih.gov/pubmed/33659799 http://dx.doi.org/10.18699/VJ20.42-o |
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