Evidence map›Paper›PMID 23240617›Full record

ArticleJournal of neurochemistry2013

Deletion or activation of the aryl hydrocarbon receptor alters adult hippocampal neurogenesis and contextual fear memory.

Sarah E Latchney, Amy M Hein, M Kerry O'Banion, Emanuel DiCicco-Bloom, Lisa A Opanashuk

Abstract read
In one paragraph

Article in Journal of neurochemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed
2.2field-weighted citation impact, top 15% 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

84 citing papers in PubMed, 138 citations in OpenAlex.

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  12. 3,3'-Diindolylmethane improves pathology and neurological outcome following traumatic brain injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
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24 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Sarah E LatchneyDepartment of Environmental Medicine, University of Rochester School of Medicine and Dentistry, Rochester, New York 14642, USA.
Amy M Hein
M Kerry O'Banion
Emanuel DiCicco-Bloom
Lisa A Opanashuk
University of Rochester · US

Funding

VISUAL INDICES OF NEUROTOXICITYP30ES001247 · NIEHS · UNIVERSITY OF ROCHESTER · PI B Paige Lawrence · 1985 to 2026
$42.8M
Training in Environment ToxicologyT32ES007026 · NIEHS · UNIVERSITY OF ROCHESTER · PI Alison Elder, Marissa Sobolewski Terry · 1985 to 2026
$20.2M
Developmental Ah receptor Activity in the CNS: Neurogenesis and NeurotoxicityR01ES016357 · NIEHS · UNIVERSITY OF ROCHESTER · PI OPANASHUK, LISA A. · 2009 to 2013
$1.7M
Training in Neuroinflammation and Glial Cell BiologyT32NS051152 · NINDS · UNIVERSITY OF ROCHESTER · PI O'BANION, M. KERRY · 2005 to 2009
$870k
NIEHS NIH HHS 30ES01247NIEHS NIH HHS P30 ES001247NIEHS NIH HHS R01 ES016357NIEHS NIH HHS R01ES016357NIEHS NIH HHS T32 ES007026NIEHS NIH HHS T32ES07026NINDS NIH HHS T32 NS051152NINDS NIH HHS T32NS051152
6 · The paper itself

Abstract

The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that mediates the toxicity of dioxin and serves multiple developmental roles. In the adult brain, while we now localize AhR mRNA to nestin-expressing neural progenitor cells in the dentate gyrus (DG) of the hippocampus, its function is unknown. This study tested the hypothesis that AhR participates in hippocampal neurogenesis and associated functions. AhR deletion and activation by the potent environmental toxicant, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), adversely impacted neurogenesis and cognition. Adult AhR-deficient mice exhibited impaired hippocampal-dependent contextual fear memory while hippocampal-independent memory remained intact. AhR-deficient mice displayed reduced cell birth, decreased cell survival, and diminished neuronal differentiation in the DG. Following TCDD exposure, wild-type mice exhibited impaired hippocampal-dependent contextual memory, decreased cell birth, reduced neuronal differentiation, and fewer mature neurons in the DG. Glial differentiation and apoptosis were not altered in either TCDD-exposed or AhR-deficient mice. Finally, defects observed in TCDD-exposed mice were dependent on AhR, as TCDD had no negative effects in AhR-deficient mice. Our findings suggest that AhR should be further evaluated as a potential transcriptional regulator of hippocampal neurogenesis and function, although other sites of action may also warrant consideration. Moreover, TCDD exposure should be considered as an environmental risk factor that disrupts adult neurogenesis and potentially related memory processes.

Indexed as

FearAdult Stem CellsAnalysis of VarianceAnimalsApoptosisBromodeoxyuridineCell DifferentiationConditioning, PsychologicalDoublecortin Domain ProteinsFemaleFlow CytometryGene Expression RegulationGlial Fibrillary Acidic ProteinGreen Fluorescent ProteinsHippocampusIntermediate Filament ProteinsBromodeoxyuridineCyan Fluorescent ProteinDoublecortin Domain ProteinsGlial Fibrillary Acidic ProteinGreen Fluorescent ProteinsIntermediate Filament ProteinsMicrotubule-Associated ProteinsNerve Tissue ProteinsNes protein, mouseNestinNeuropeptidesPolychlorinated DibenzodioxinsReceptors, Aryl Hydrocarbon

Identifiers

PMID23240617
PMCPMC4540228
OpenAlexW1963687870

What OpenQuestion holds

Textmetadata
LicenceTDM
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.