Evidence map›Paper›PMID 24952232›Full record

ArticleNeurotoxicology2014

Fluoxetine treatment ameliorates depression induced by perinatal arsenic exposure via a neurogenic mechanism.

Christina R Tyler, Benjamin R Solomon, Adam L Ulibarri, Andrea M Allan

Open access · greenAbstract read
In one paragraph

Article in Neurotoxicology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 21% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.

  1. Pooled it
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  5. D1R-5-HT2AR Uncoupling Reduces Depressive Behaviours via HDAC Signalling.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023
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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

4 authors at 1 institution in 1 country.

Christina R TylerDepartment of Neurosciences, School of Medicine, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA.
Benjamin R SolomonDepartment of Neurosciences, School of Medicine, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA.
Adam L UlibarriDepartment of Neurosciences, School of Medicine, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA.
Andrea M AllanDepartment of Neurosciences, School of Medicine, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA. Electronic address: aallan@salud.unm.edu.
University of New Mexico · US

Funding

Prenatal arsenic exposure alters transcriptional, post-transcriptional and post-translational programming of the glucocorticoid system in a sexually dimorphic mannerR01ES019583 · NIEHS · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI ALLAN, ANDREA M · 2011 to 2021
$3.3M
The epigenetic link between environmental exposure and adult onset depressionF31MH101984 · NIMH · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI TYLER, CHRISTINA RENE · 2013 to 2014
$43k
NIEHS NIH HHS R01 ES019583NIEHS NIH HHS R01ES019583NIMH NIH HHS F31 MH 101984NIMH NIH HHS F31 MH101984
6 · The paper itself

Abstract

Several epidemiological studies have reported an association between arsenic exposure and increased rates of psychiatric disorders, including depression, in exposed populations. We have previously demonstrated that developmental exposure to low amounts of arsenic induces depression in adulthood along with several morphological and molecular aberrations, particularly associated with the hippocampus and the hypothalamic-pituitary-adrenal (HPA) axis. The extent and potential reversibility of this toxin-induced damage has not been characterized to date. In this study, we assessed the effects of fluoxetine, a selective serotonin reuptake inhibitor antidepressant, on adult animals exposed to arsenic during development. Perinatal arsenic exposure (PAE) induced depressive-like symptoms in a mild learned helplessness task and in the forced swim task after acute exposure to a predator odor (2,4,5-trimethylthiazoline, TMT). Chronic fluoxetine treatment prevented these behaviors in both tasks in arsenic-exposed animals and ameliorated arsenic-induced blunted stress responses, as measured by corticosterone (CORT) levels before and after TMT exposure. Morphologically, chronic fluoxetine treatment reversed deficits in adult hippocampal neurogenesis (AHN) after PAE, specifically differentiation and survival of neural progenitor cells. Protein expression of BDNF, CREB, the glucocorticoid receptor (GR), and HDAC2 was significantly increased in the dentate gyrus of arsenic animals after fluoxetine treatment. This study demonstrates that damage induced by perinatal arsenic exposure is reversible with chronic fluoxetine treatment resulting in restored resiliency to depression via a neurogenic mechanism.

Indexed as

AnimalsAntidepressive Agents, Second-GenerationArsenicDepressionFemaleFluoxetineHelplessness, LearnedHippocampusMaleMiceMice, Inbred C57BLMotor ActivityNeurogenesisPregnancyPrenatal Exposure Delayed EffectsSelective Serotonin Reuptake InhibitorsAntidepressive Agents, Second-GenerationArsenicFluoxetineSelective Serotonin Reuptake InhibitorsArsenicFluoxetineNeurogenesisPsychiatric disordersStress

Identifiers

PMID24952232
PMCPMC4180420
OpenAlexW1981285433

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.