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The Neuronal Glutamate Transporter EAAT3 in Obsessive-Compulsive Disorder

Obsessive compulsive disorder (OCD) is a heterogeneous psychiatric disorder affecting 1%–3% of the population worldwide. About half of OCD afflicted individuals do not respond to currently available pharmacotherapy, which is mainly based on serotonin reuptake inhibition. Therefore, there is a critic...

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Autores principales: Escobar, Angélica P., Wendland, Jens R., Chávez, Andrés E., Moya, Pablo R.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6872633/
https://www.ncbi.nlm.nih.gov/pubmed/31803055
http://dx.doi.org/10.3389/fphar.2019.01362
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author Escobar, Angélica P.
Wendland, Jens R.
Chávez, Andrés E.
Moya, Pablo R.
author_facet Escobar, Angélica P.
Wendland, Jens R.
Chávez, Andrés E.
Moya, Pablo R.
author_sort Escobar, Angélica P.
collection PubMed
description Obsessive compulsive disorder (OCD) is a heterogeneous psychiatric disorder affecting 1%–3% of the population worldwide. About half of OCD afflicted individuals do not respond to currently available pharmacotherapy, which is mainly based on serotonin reuptake inhibition. Therefore, there is a critical need to search novel and improved therapeutic targets to treat this devastating disorder. In recent years, accumulating evidence has supported the glutamatergic hypothesis of OCD, and particularly pointing a potential role for the neuronal glutamate transporter EAAT3. This mini-review summarizes recent findings regarding the neurobiological basis of OCD, with an emphasis on the glutamatergic neurotransmission and EAAT3 as a key player in OCD etiology.
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spelling pubmed-68726332019-12-04 The Neuronal Glutamate Transporter EAAT3 in Obsessive-Compulsive Disorder Escobar, Angélica P. Wendland, Jens R. Chávez, Andrés E. Moya, Pablo R. Front Pharmacol Pharmacology Obsessive compulsive disorder (OCD) is a heterogeneous psychiatric disorder affecting 1%–3% of the population worldwide. About half of OCD afflicted individuals do not respond to currently available pharmacotherapy, which is mainly based on serotonin reuptake inhibition. Therefore, there is a critical need to search novel and improved therapeutic targets to treat this devastating disorder. In recent years, accumulating evidence has supported the glutamatergic hypothesis of OCD, and particularly pointing a potential role for the neuronal glutamate transporter EAAT3. This mini-review summarizes recent findings regarding the neurobiological basis of OCD, with an emphasis on the glutamatergic neurotransmission and EAAT3 as a key player in OCD etiology. Frontiers Media S.A. 2019-11-15 /pmc/articles/PMC6872633/ /pubmed/31803055 http://dx.doi.org/10.3389/fphar.2019.01362 Text en Copyright © 2019 Escobar, Wendland, Chávez and Moya http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Pharmacology
Escobar, Angélica P.
Wendland, Jens R.
Chávez, Andrés E.
Moya, Pablo R.
The Neuronal Glutamate Transporter EAAT3 in Obsessive-Compulsive Disorder
title The Neuronal Glutamate Transporter EAAT3 in Obsessive-Compulsive Disorder
title_full The Neuronal Glutamate Transporter EAAT3 in Obsessive-Compulsive Disorder
title_fullStr The Neuronal Glutamate Transporter EAAT3 in Obsessive-Compulsive Disorder
title_full_unstemmed The Neuronal Glutamate Transporter EAAT3 in Obsessive-Compulsive Disorder
title_short The Neuronal Glutamate Transporter EAAT3 in Obsessive-Compulsive Disorder
title_sort neuronal glutamate transporter eaat3 in obsessive-compulsive disorder
topic Pharmacology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6872633/
https://www.ncbi.nlm.nih.gov/pubmed/31803055
http://dx.doi.org/10.3389/fphar.2019.01362
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