Cargando…

mGluR5 Ablation in Cortical Glutamatergic Neurons Increases Novelty-Induced Locomotion

The group I metabotropic glutamate receptor 5 (mGluR5) has been implicated in the pathology of various neurological disorders including schizophrenia, ADHD, and autism. mGluR5-dependent synaptic plasticity has been described at a variety of neural connections and its signaling has been implicated in...

Descripción completa

Detalles Bibliográficos
Autores principales: Jew, Chris P., Wu, Chia-Shan, Sun, Hao, Zhu, Jie, Huang, Jui-Yen, Yu, Dinghui, Justice, Nicholas J., Lu, Hui-Chen
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3734292/
https://www.ncbi.nlm.nih.gov/pubmed/23940572
http://dx.doi.org/10.1371/journal.pone.0070415
_version_ 1782279516493709312
author Jew, Chris P.
Wu, Chia-Shan
Sun, Hao
Zhu, Jie
Huang, Jui-Yen
Yu, Dinghui
Justice, Nicholas J.
Lu, Hui-Chen
author_facet Jew, Chris P.
Wu, Chia-Shan
Sun, Hao
Zhu, Jie
Huang, Jui-Yen
Yu, Dinghui
Justice, Nicholas J.
Lu, Hui-Chen
author_sort Jew, Chris P.
collection PubMed
description The group I metabotropic glutamate receptor 5 (mGluR5) has been implicated in the pathology of various neurological disorders including schizophrenia, ADHD, and autism. mGluR5-dependent synaptic plasticity has been described at a variety of neural connections and its signaling has been implicated in several behaviors. These behaviors include locomotor reactivity to novel environment, sensorimotor gating, anxiety, and cognition. mGluR5 is expressed in glutamatergic neurons, inhibitory neurons, and glia in various brain regions. In this study, we show that deleting mGluR5 expression only in principal cortical neurons leads to defective cannabinoid receptor 1 (CB1R) dependent synaptic plasticity in the prefrontal cortex. These cortical glutamatergic mGluR5 knockout mice exhibit increased novelty-induced locomotion, and their locomotion can be further enhanced by treatment with the psychostimulant methylphenidate. Despite a modest reduction in repetitive behaviors, cortical glutamatergic mGluR5 knockout mice are normal in sensorimotor gating, anxiety, motor balance/learning and fear conditioning behaviors. These results show that mGluR5 signaling in cortical glutamatergic neurons is required for precisely modulating locomotor reactivity to a novel environment but not for sensorimotor gating, anxiety, motor coordination, several forms of learning or social interactions.
format Online
Article
Text
id pubmed-3734292
institution National Center for Biotechnology Information
language English
publishDate 2013
publisher Public Library of Science
record_format MEDLINE/PubMed
spelling pubmed-37342922013-08-12 mGluR5 Ablation in Cortical Glutamatergic Neurons Increases Novelty-Induced Locomotion Jew, Chris P. Wu, Chia-Shan Sun, Hao Zhu, Jie Huang, Jui-Yen Yu, Dinghui Justice, Nicholas J. Lu, Hui-Chen PLoS One Research Article The group I metabotropic glutamate receptor 5 (mGluR5) has been implicated in the pathology of various neurological disorders including schizophrenia, ADHD, and autism. mGluR5-dependent synaptic plasticity has been described at a variety of neural connections and its signaling has been implicated in several behaviors. These behaviors include locomotor reactivity to novel environment, sensorimotor gating, anxiety, and cognition. mGluR5 is expressed in glutamatergic neurons, inhibitory neurons, and glia in various brain regions. In this study, we show that deleting mGluR5 expression only in principal cortical neurons leads to defective cannabinoid receptor 1 (CB1R) dependent synaptic plasticity in the prefrontal cortex. These cortical glutamatergic mGluR5 knockout mice exhibit increased novelty-induced locomotion, and their locomotion can be further enhanced by treatment with the psychostimulant methylphenidate. Despite a modest reduction in repetitive behaviors, cortical glutamatergic mGluR5 knockout mice are normal in sensorimotor gating, anxiety, motor balance/learning and fear conditioning behaviors. These results show that mGluR5 signaling in cortical glutamatergic neurons is required for precisely modulating locomotor reactivity to a novel environment but not for sensorimotor gating, anxiety, motor coordination, several forms of learning or social interactions. Public Library of Science 2013-08-05 /pmc/articles/PMC3734292/ /pubmed/23940572 http://dx.doi.org/10.1371/journal.pone.0070415 Text en © 2013 Jew et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
Jew, Chris P.
Wu, Chia-Shan
Sun, Hao
Zhu, Jie
Huang, Jui-Yen
Yu, Dinghui
Justice, Nicholas J.
Lu, Hui-Chen
mGluR5 Ablation in Cortical Glutamatergic Neurons Increases Novelty-Induced Locomotion
title mGluR5 Ablation in Cortical Glutamatergic Neurons Increases Novelty-Induced Locomotion
title_full mGluR5 Ablation in Cortical Glutamatergic Neurons Increases Novelty-Induced Locomotion
title_fullStr mGluR5 Ablation in Cortical Glutamatergic Neurons Increases Novelty-Induced Locomotion
title_full_unstemmed mGluR5 Ablation in Cortical Glutamatergic Neurons Increases Novelty-Induced Locomotion
title_short mGluR5 Ablation in Cortical Glutamatergic Neurons Increases Novelty-Induced Locomotion
title_sort mglur5 ablation in cortical glutamatergic neurons increases novelty-induced locomotion
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3734292/
https://www.ncbi.nlm.nih.gov/pubmed/23940572
http://dx.doi.org/10.1371/journal.pone.0070415
work_keys_str_mv AT jewchrisp mglur5ablationincorticalglutamatergicneuronsincreasesnoveltyinducedlocomotion
AT wuchiashan mglur5ablationincorticalglutamatergicneuronsincreasesnoveltyinducedlocomotion
AT sunhao mglur5ablationincorticalglutamatergicneuronsincreasesnoveltyinducedlocomotion
AT zhujie mglur5ablationincorticalglutamatergicneuronsincreasesnoveltyinducedlocomotion
AT huangjuiyen mglur5ablationincorticalglutamatergicneuronsincreasesnoveltyinducedlocomotion
AT yudinghui mglur5ablationincorticalglutamatergicneuronsincreasesnoveltyinducedlocomotion
AT justicenicholasj mglur5ablationincorticalglutamatergicneuronsincreasesnoveltyinducedlocomotion
AT luhuichen mglur5ablationincorticalglutamatergicneuronsincreasesnoveltyinducedlocomotion