Role of Glutamatergic Projections from the Ventral CA1 to Infralimbic Cortex in Context-Induced Reinstatement of Heroin Seeking

The prelimbic cortex (PL) and infralimbic cortex (IL) play a role in context-induced reinstatement of heroin seeking in an animal model of drug relapse. Both the PL and IL receive direct glutamatergic projections from the ventral CA1 (vCA1), which is also involved in context-induced reinstatement of...

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Autores principales: Wang, Na, Ge, Feifei, Cui, Cailian, Li, Yijing, Sun, Xiaowei, Sun, Linlin, Wang, Xinjuan, Liu, Shuli, Zhang, Haolin, Liu, Yan, Jia, Meng, Yang, Mingda
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2018
Materias:
Original Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5916356/
https://www.ncbi.nlm.nih.gov/pubmed/29134962
http://dx.doi.org/10.1038/npp.2017.279
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author Wang, Na
Ge, Feifei
Cui, Cailian
Li, Yijing
Sun, Xiaowei
Sun, Linlin
Wang, Xinjuan
Liu, Shuli
Zhang, Haolin
Liu, Yan
Jia, Meng
Yang, Mingda
author_facet Wang, Na
Ge, Feifei
Cui, Cailian
Li, Yijing
Sun, Xiaowei
Sun, Linlin
Wang, Xinjuan
Liu, Shuli
Zhang, Haolin
Liu, Yan
Jia, Meng
Yang, Mingda
author_sort Wang, Na
collection PubMed
description The prelimbic cortex (PL) and infralimbic cortex (IL) play a role in context-induced reinstatement of heroin seeking in an animal model of drug relapse. Both the PL and IL receive direct glutamatergic projections from the ventral CA1 (vCA1), which is also involved in context-induced reinstatement of cocaine and heroin seeking. Here we studied the role of vCA1-PL and vCA1-IL projections in context-induced reinstatement of heroin seeking by using electrophysiological, neuropharmacological, chemogenetic, and molecular methods. We showed that context-induced reinstatement of heroin seeking caused selective activation of the vCA1-IL but not vCA1-PL glutamatergic projections, decreased synaptosomal GluA2 expression in the IL, impaired basal synaptic transmission, and facilitation of long-term depression (LTD) in the vCA1-IL pathway. Additionally, chemogenetic inactivation of the vCA1-IL but not vCA1-PL pathway decreased context-induced reinstatement of heroin seeking. Inactivation of the vCA1-IL pathway also reversed synaptosomal GluA2 downregulation and basal transmission reduction, and blocked LTD induction. Taken together, our results demonstrate a critical role of the vCA1-IL glutamatergic projection in context-induced reinstatement of heroin seeking in a rat model of drug relapse.
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spelling pubmed-59163562018-05-01 Role of Glutamatergic Projections from the Ventral CA1 to Infralimbic Cortex in Context-Induced Reinstatement of Heroin Seeking Wang, Na Ge, Feifei Cui, Cailian Li, Yijing Sun, Xiaowei Sun, Linlin Wang, Xinjuan Liu, Shuli Zhang, Haolin Liu, Yan Jia, Meng Yang, Mingda Neuropsychopharmacology Original Article The prelimbic cortex (PL) and infralimbic cortex (IL) play a role in context-induced reinstatement of heroin seeking in an animal model of drug relapse. Both the PL and IL receive direct glutamatergic projections from the ventral CA1 (vCA1), which is also involved in context-induced reinstatement of cocaine and heroin seeking. Here we studied the role of vCA1-PL and vCA1-IL projections in context-induced reinstatement of heroin seeking by using electrophysiological, neuropharmacological, chemogenetic, and molecular methods. We showed that context-induced reinstatement of heroin seeking caused selective activation of the vCA1-IL but not vCA1-PL glutamatergic projections, decreased synaptosomal GluA2 expression in the IL, impaired basal synaptic transmission, and facilitation of long-term depression (LTD) in the vCA1-IL pathway. Additionally, chemogenetic inactivation of the vCA1-IL but not vCA1-PL pathway decreased context-induced reinstatement of heroin seeking. Inactivation of the vCA1-IL pathway also reversed synaptosomal GluA2 downregulation and basal transmission reduction, and blocked LTD induction. Taken together, our results demonstrate a critical role of the vCA1-IL glutamatergic projection in context-induced reinstatement of heroin seeking in a rat model of drug relapse. Nature Publishing Group 2018-05 2017-12-20 /pmc/articles/PMC5916356/ /pubmed/29134962 http://dx.doi.org/10.1038/npp.2017.279 Text en Copyright © 2018 The Author(s) http://creativecommons.org/licenses/by-nc-nd/4.0/ This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/4.0/
spellingShingle Original Article
Wang, Na
Ge, Feifei
Cui, Cailian
Li, Yijing
Sun, Xiaowei
Sun, Linlin
Wang, Xinjuan
Liu, Shuli
Zhang, Haolin
Liu, Yan
Jia, Meng
Yang, Mingda
Role of Glutamatergic Projections from the Ventral CA1 to Infralimbic Cortex in Context-Induced Reinstatement of Heroin Seeking
title Role of Glutamatergic Projections from the Ventral CA1 to Infralimbic Cortex in Context-Induced Reinstatement of Heroin Seeking
title_full Role of Glutamatergic Projections from the Ventral CA1 to Infralimbic Cortex in Context-Induced Reinstatement of Heroin Seeking
title_fullStr Role of Glutamatergic Projections from the Ventral CA1 to Infralimbic Cortex in Context-Induced Reinstatement of Heroin Seeking
title_full_unstemmed Role of Glutamatergic Projections from the Ventral CA1 to Infralimbic Cortex in Context-Induced Reinstatement of Heroin Seeking
title_short Role of Glutamatergic Projections from the Ventral CA1 to Infralimbic Cortex in Context-Induced Reinstatement of Heroin Seeking
title_sort role of glutamatergic projections from the ventral ca1 to infralimbic cortex in context-induced reinstatement of heroin seeking
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5916356/
https://www.ncbi.nlm.nih.gov/pubmed/29134962
http://dx.doi.org/10.1038/npp.2017.279
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