Evidence map›Paper›PMID 26640238›Full record

ArticleToxicology letters2016

Role of glutamate receptors in tetrabrominated diphenyl ether (BDE-47) neurotoxicity in mouse cerebellar granule neurons.

Lucio G Costa, Sara Tagliaferri, Pamela J Roqué, Claudia Pellacani

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Toxicology letters, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.5field-weighted citation impact, top 12% 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

11 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Toxic Effects and Mechanisms of Polybrominated Diphenyl Ethers.International journal of molecular sciences · 2023
    Review
  6. Article
  7. Gene×environment interactions in autism spectrum disorders.Current topics in developmental biology · 2023
    Review
  8. Article
  9. Review
  10. Article
  11. 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

4 authors at 2 institutions in 2 countries.

Lucio G CostaDept. of Environmental and Occupational Health Sciences, University of Washington, Seattle, WA, USA; Dept. of Neuroscience, University of Parma, Parma, Italy. Electronic address: lgcosta@u.washington.edu.
Sara TagliaferriDept. of Environmental and Occupational Health Sciences, University of Washington, Seattle, WA, USA; Dept. of Neuroscience, University of Parma, Parma, Italy.
Pamela J RoquéDept. of Environmental and Occupational Health Sciences, University of Washington, Seattle, WA, USA.
Claudia PellacaniDept. of Neuroscience, University of Parma, Parma, Italy.
University of Washington · USUniversity of Parma · IT

Funding

XENOBIOTIC BIOTRANSFORMATION AND DISPOSITIONP30ES007033 · NIEHS · UNIVERSITY OF WASHINGTON · PI ALI SHOJAIE · 1995 to 2026
$42.5M
Intellectual and Developmental Disabilities Research CenterU54HD083091 · NICHD · UNIVERSITY OF WASHINGTON · PI GARDEN, GWENN A · 2014 to 2019
$7.9M
Low level exposure to PBDEs: testing the hormetic and epigenetic hypothesesR21ES022611 · NIEHS · UNIVERSITY OF WASHINGTON · PI COSTA, LUCIO G · 2013 to 2014
$423k
NICHD NIH HHS U54 HD083091NIEHS NIH HHS P30 ES007033NIEHS NIH HHS P30ES07033NIEHS NIH HHS R21 ES022611NIEHS NIH HHS R21ES22611
6 · The paper itself

Abstract

The polybrominated diphenyl ether (PBDE) flame retardants are developmental neurotoxicants, as evidenced by numerous in vitro, animal and human studies. PBDEs can alter the homeostasis of thyroid hormone and directly interact with brain cells. Induction of oxidative stress, leading to DNA damage and apoptotic cell death is a prominent mechanism of PBDE neurotoxicity, though other mechanisms have also been suggested. In the present study we investigated the potential role played by glutamate receptors in the in vitro neurotoxicity of the tetrabromodiphenyl ether BDE-47, one of the most abundant PBDE congeners. Toxicity of BDE-47 in mouse cerebellar neurons was diminished by antagonists of glutamate ionotropic receptors, but not by antagonists of glutamate metabotropic receptors. Antagonists of NMDA and AMPA/Kainate receptors also inhibited BDE-47-induced oxidative stress and increases in intracellular calcium. The calcium chelator BAPTA-AM also inhibited BDE-47 cytotoxicity and oxidative stress. BDE-47 caused a rapid increase of extracellular glutamate levels, which was not antagonized by any of the compounds tested. The results suggest that BDE-47, by still unknown mechanisms, increases extracellular glutamate which in turn activates ionotropic glutamate receptors leading to increased calcium levels, oxidative stress, and ultimately cell death.

Indexed as

AnimalsCalciumCell DeathCerebellumChelating AgentsCytoplasmic GranulesEgtazic AcidExcitatory Amino Acid AntagonistsFlame RetardantsHalogenated Diphenyl EthersMiceMice, Inbred C57BLNeuronsNeurotoxicity SyndromesOxidative StressReceptors, AMPA1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester2,2',4,4'-tetrabromodiphenyl etherCalciumChelating AgentsEgtazic AcidExcitatory Amino Acid AntagonistsFlame RetardantsHalogenated Diphenyl EthersReceptors, AMPAReceptors, GlutamateReceptors, Ionotropic GlutamateReceptors, Metabotropic GlutamateReceptors, N-Methyl-D-AspartateAMPA/KainateBDE-47Developmental neurotoxicityFlame retardantsGlutamate receptorsNMDA

Identifiers

PMID26640238
PMCPMC4691362
OpenAlexW2232152495

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.