Evidence map›Paper›PMID 36607593›Full record

ReviewNeurotoxicity research2023

Aryl Hydrocarbon Receptor in Glia Cells: A Plausible Glutamatergic Neurotransmission Orchestrator.

Janisse Silva-Parra, Cristina Sandu, Marie-Paule Felder-Schmittbuhl, Luisa C Hernández-Kelly, Arturo Ortega

Open access · greenAbstract readReview
PubMed Publisher
In one paragraph

Review in Neurotoxicity research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.4field-weighted citation impact, top 44% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 2 countries.

Janisse Silva-ParraDepartamento de Toxicología, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, Av. IPN 2508, San Pedro Zacatenco, 07360, CDMX, México.ORCID http://orcid.org/0000-0002-2289-1401
Cristina SanduCentre National de la Recherche Scientifique, Institut des Neurosciences Cellulaires et Intégratives, Université de Strasbourg, Strasbourg, France.
Marie-Paule Felder-SchmittbuhlCentre National de la Recherche Scientifique, Institut des Neurosciences Cellulaires et Intégratives, Université de Strasbourg, Strasbourg, France.ORCID http://orcid.org/0000-0003-3539-1243
Luisa C Hernández-KellyDepartamento de Toxicología, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, Av. IPN 2508, San Pedro Zacatenco, 07360, CDMX, México.ORCID http://orcid.org/0000-0003-2710-3731
Arturo OrtegaDepartamento de Toxicología, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, Av. IPN 2508, San Pedro Zacatenco, 07360, CDMX, México. arortega@cinvestav.mx.ORCID http://orcid.org/0000-0002-9594-8114
Instituto Politécnico Nacional · MXInstitut des Neurosciences Cellulaires et Intégratives · FR

Funding

Consejo Nacional de Ciencia y Tecnología 255087Consejo Nacional de Ciencia y Tecnología 315689Consejo Nacional de Ciencia y Tecnología 735674
6 · The paper itself

Abstract

Glutamate is the major excitatory amino acid in the vertebrate brain. Glutamatergic signaling is involved in most of the central nervous system functions. Its main components, namely receptors, ion channels, and transporters, are tightly regulated at the transcriptional, translational, and post-translational levels through a diverse array of extracellular signals, such as food, light, and neuroactive molecules. An exquisite and well-coordinated glial/neuronal bidirectional communication is required for proper excitatory amino acid signal transactions. Biochemical shuttles such as the glutamate/glutamine and the astrocyte-neuronal lactate represent the fundamental involvement of glial cells in glutamatergic transmission. In fact, the disruption of any of these coordinated biochemical intercellular cascades leads to an excitotoxic insult that underlies some aspects of most of the neurodegenerative diseases characterized thus far. In this contribution, we provide a comprehensive summary of the involvement of the Aryl hydrocarbon receptor, a ligand-dependent transcription factor in the gene expression regulation of glial glutamate transporters. These receptors might serve as potential targets for the development of novel strategies for the treatment of neurodegenerative diseases.

Indexed as

NeurogliaReceptors, Aryl HydrocarbonSynaptic TransmissionGlutamic AcidSignal TransductionGlutamic AcidReceptors, Aryl HydrocarbonAryl hydrocarbon receptorGlutamate transportersKynurenic acid, Circadian rhythmsRadial glia

Identifiers

PMID36607593
OpenAlexW4313647695

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.