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Striatal Syntaxin 1A Is Associated with Development of Tourette Syndrome in an Iminodipropionitrile-Induced Animal Model
Tourette syndrome (TS) is a neurodevelopmental movement disorder characterized by multiple motor and vocal tics. In this study, we used a TS rat model induced by 3,3′-iminodipropionitrile (IDPN) and aimed to investigate the expression change of Syntaxin 1A (STX1A). Rats in the control group received...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9492347/ https://www.ncbi.nlm.nih.gov/pubmed/36157213 http://dx.doi.org/10.1155/2022/1148191 |
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author | Yang, Liu Wang, Xueming Liu, Xiumei Chen, Xin |
author_facet | Yang, Liu Wang, Xueming Liu, Xiumei Chen, Xin |
author_sort | Yang, Liu |
collection | PubMed |
description | Tourette syndrome (TS) is a neurodevelopmental movement disorder characterized by multiple motor and vocal tics. In this study, we used a TS rat model induced by 3,3′-iminodipropionitrile (IDPN) and aimed to investigate the expression change of Syntaxin 1A (STX1A). Rats in the control group received intraperitoneal injection of normal saline, and TS rats were injected with IDPN (150 mg/kg/day). After 7 days of treatment, the stereotypic behaviors were assessed. Next, rats were sacrificed; brains were removed for RNA extraction and Western blotting analysis and fixed in 4% paraformaldehyde for immunofluorescence analysis. After 7 days of IDPN administration, stereotypic behaviors were successfully induced. The IDPN group exhibited more counts in biting, putting forepaws around mouth, licking, head twitching, shaking claws, body raising, and episodic utterance. The striatal STX1A mRNA, protein, and STX1A expression in striatal dopaminergic neurons were investigated. As expected, the total STX1A mRNA and protein levels were decreased in the TS model rats. In the striatal dopaminergic neurons, the IDPN group showed a slightly decreased STX1A/TH double positive area, but no statistical significance was found. Additionally, we assessed the expression of some genes closely related to STX1A, such as SNAP25, SY, and gephyrin, and no differences were found between the two groups. Together, reduced STX1A expression is associated with IDPN-induced TS development. Our findings suggested that decreased striatal STX1A expression is associated with the development of TS in the IDPN-induced rat model. |
format | Online Article Text |
id | pubmed-9492347 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-94923472022-09-22 Striatal Syntaxin 1A Is Associated with Development of Tourette Syndrome in an Iminodipropionitrile-Induced Animal Model Yang, Liu Wang, Xueming Liu, Xiumei Chen, Xin Dis Markers Research Article Tourette syndrome (TS) is a neurodevelopmental movement disorder characterized by multiple motor and vocal tics. In this study, we used a TS rat model induced by 3,3′-iminodipropionitrile (IDPN) and aimed to investigate the expression change of Syntaxin 1A (STX1A). Rats in the control group received intraperitoneal injection of normal saline, and TS rats were injected with IDPN (150 mg/kg/day). After 7 days of treatment, the stereotypic behaviors were assessed. Next, rats were sacrificed; brains were removed for RNA extraction and Western blotting analysis and fixed in 4% paraformaldehyde for immunofluorescence analysis. After 7 days of IDPN administration, stereotypic behaviors were successfully induced. The IDPN group exhibited more counts in biting, putting forepaws around mouth, licking, head twitching, shaking claws, body raising, and episodic utterance. The striatal STX1A mRNA, protein, and STX1A expression in striatal dopaminergic neurons were investigated. As expected, the total STX1A mRNA and protein levels were decreased in the TS model rats. In the striatal dopaminergic neurons, the IDPN group showed a slightly decreased STX1A/TH double positive area, but no statistical significance was found. Additionally, we assessed the expression of some genes closely related to STX1A, such as SNAP25, SY, and gephyrin, and no differences were found between the two groups. Together, reduced STX1A expression is associated with IDPN-induced TS development. Our findings suggested that decreased striatal STX1A expression is associated with the development of TS in the IDPN-induced rat model. Hindawi 2022-09-14 /pmc/articles/PMC9492347/ /pubmed/36157213 http://dx.doi.org/10.1155/2022/1148191 Text en Copyright © 2022 Liu Yang et al. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Yang, Liu Wang, Xueming Liu, Xiumei Chen, Xin Striatal Syntaxin 1A Is Associated with Development of Tourette Syndrome in an Iminodipropionitrile-Induced Animal Model |
title | Striatal Syntaxin 1A Is Associated with Development of Tourette Syndrome in an Iminodipropionitrile-Induced Animal Model |
title_full | Striatal Syntaxin 1A Is Associated with Development of Tourette Syndrome in an Iminodipropionitrile-Induced Animal Model |
title_fullStr | Striatal Syntaxin 1A Is Associated with Development of Tourette Syndrome in an Iminodipropionitrile-Induced Animal Model |
title_full_unstemmed | Striatal Syntaxin 1A Is Associated with Development of Tourette Syndrome in an Iminodipropionitrile-Induced Animal Model |
title_short | Striatal Syntaxin 1A Is Associated with Development of Tourette Syndrome in an Iminodipropionitrile-Induced Animal Model |
title_sort | striatal syntaxin 1a is associated with development of tourette syndrome in an iminodipropionitrile-induced animal model |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9492347/ https://www.ncbi.nlm.nih.gov/pubmed/36157213 http://dx.doi.org/10.1155/2022/1148191 |
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