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The Aryl Hydrocarbon Receptor and the Nervous System

The aryl hydrocarbon receptor (or AhR) is a cytoplasmic receptor of pollutants. It translocates into the nucleus upon binding to its ligands, and forms a heterodimer with ARNT (AhR nuclear translocator). The heterodimer is a transcription factor, which regulates the transcription of xenobiotic metab...

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Autores principales: Juricek, Ludmila, Coumoul, Xavier
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6163841/
https://www.ncbi.nlm.nih.gov/pubmed/30149528
http://dx.doi.org/10.3390/ijms19092504
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author Juricek, Ludmila
Coumoul, Xavier
author_facet Juricek, Ludmila
Coumoul, Xavier
author_sort Juricek, Ludmila
collection PubMed
description The aryl hydrocarbon receptor (or AhR) is a cytoplasmic receptor of pollutants. It translocates into the nucleus upon binding to its ligands, and forms a heterodimer with ARNT (AhR nuclear translocator). The heterodimer is a transcription factor, which regulates the transcription of xenobiotic metabolizing enzymes. Expressed in many cells in vertebrates, it is mostly present in neuronal cell types in invertebrates, where it regulates dendritic morphology or feeding behavior. Surprisingly, few investigations have been conducted to unravel the function of the AhR in the central or peripheral nervous systems of vertebrates. In this review, we will present how the AhR regulates neural functions in both invertebrates and vertebrates as deduced mainly from the effects of xenobiotics. We will introduce some of the molecular mechanisms triggered by the well-known AhR ligand, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), which impact on neuronal proliferation, differentiation, and survival. Finally, we will point out the common features found in mice that are exposed to pollutants, and in AhR knockout mice.
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spelling pubmed-61638412018-10-10 The Aryl Hydrocarbon Receptor and the Nervous System Juricek, Ludmila Coumoul, Xavier Int J Mol Sci Review The aryl hydrocarbon receptor (or AhR) is a cytoplasmic receptor of pollutants. It translocates into the nucleus upon binding to its ligands, and forms a heterodimer with ARNT (AhR nuclear translocator). The heterodimer is a transcription factor, which regulates the transcription of xenobiotic metabolizing enzymes. Expressed in many cells in vertebrates, it is mostly present in neuronal cell types in invertebrates, where it regulates dendritic morphology or feeding behavior. Surprisingly, few investigations have been conducted to unravel the function of the AhR in the central or peripheral nervous systems of vertebrates. In this review, we will present how the AhR regulates neural functions in both invertebrates and vertebrates as deduced mainly from the effects of xenobiotics. We will introduce some of the molecular mechanisms triggered by the well-known AhR ligand, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), which impact on neuronal proliferation, differentiation, and survival. Finally, we will point out the common features found in mice that are exposed to pollutants, and in AhR knockout mice. MDPI 2018-08-24 /pmc/articles/PMC6163841/ /pubmed/30149528 http://dx.doi.org/10.3390/ijms19092504 Text en © 2018 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Juricek, Ludmila
Coumoul, Xavier
The Aryl Hydrocarbon Receptor and the Nervous System
title The Aryl Hydrocarbon Receptor and the Nervous System
title_full The Aryl Hydrocarbon Receptor and the Nervous System
title_fullStr The Aryl Hydrocarbon Receptor and the Nervous System
title_full_unstemmed The Aryl Hydrocarbon Receptor and the Nervous System
title_short The Aryl Hydrocarbon Receptor and the Nervous System
title_sort aryl hydrocarbon receptor and the nervous system
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6163841/
https://www.ncbi.nlm.nih.gov/pubmed/30149528
http://dx.doi.org/10.3390/ijms19092504
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