Evidence map›Paper›PMID 21073715›Full record

ArticleJournal of biomedical science2010

Prenatal exposure of ethanol induces increased glutamatergic neuronal differentiation of neural progenitor cells.

Ki Chan Kim, Hyo Sang Go, Hae Rang Bak, Chang Soon Choi, Inha Choi, Pitna Kim, Seol-Heui Han, So Min Han, Chan Young Shin, Kwang Ho Ko

Open access · diamondAbstract read
In one paragraph

Article in Journal of biomedical science, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
4.2field-weighted citation impact, top 7% 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

18 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
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  4. Upregulated GIRK2 Counteracts Ethanol-Induced Changes in Excitability and Respiration in Human Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
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  11. Stem cell therapy: a new approach to the treatment of refractory depression.Journal of neural transmission (Vienna, Austria : 1996) · 2014
    Article
  12. Article
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  15. Review
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  17. Article
  18. Developmental changes in embryonic hypothalamic neurons during prenatal fat exposure.American journal of physiology. Endocrinology and metabolism · 2012
    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

10 authors at 2 institutions in 1 country.

Ki Chan KimDepartment of Pharmacology, College of Pharmacy, Seoul National University, Seoul, Korea.
Hyo Sang Go
Hae Rang Bak
Chang Soon Choi
Inha Choi
Pitna Kim
Seol-Heui Han
So Min Han
Chan Young Shin
Kwang Ho Ko
Konkuk University · KRSeoul National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPrenatal ethanol exposure during pregnancy induces a spectrum of mental and physical disorders called fetal alcohol spectrum disorder (FASD). The central nervous system is the main organ influenced by FASD, and neurological symptoms include mental retardation, learning abnormalities, hyperactivity and seizure susceptibility in childhood along with the microcephaly. In this study, we examined whether ethanol exposure adversely affects the proliferation of NPC and de-regulates the normal ratio between glutamatergic and GABAergic neuronal differentiation using primary neural progenitor culture (NPC) and in vivo FASD models.

methodsNeural progenitor cells were cultured from E14 embryo brain of Sprague-Dawley rat. Pregnant mice and rats were treated with ethanol (2 or 4 g/kg/day) diluted with normal saline from E7 to E16 for in vivo FASD animal models. Expression level of proteins was investigated by western blot analysis and immunocytochemical assays. MTT was used for cell viability. Proliferative activity of NPCs was identified by BrdU incorporation, immunocytochemistry and FACS analysis.

resultsReduced proliferation of NPCs by ethanol was demonstrated using BrdU incorporation, immunocytochemistry and FACS analysis. In addition, ethanol induced the imbalance between glutamatergic and GABAergic neuronal differentiation via transient increase in the expression of Pax6, Ngn2 and NeuroD with concomitant decrease in the expression of Mash1. Similar pattern of expression of those transcription factors was observed using an in vivo model of FASD as well as the increased expression of PSD-95 and decreased expression of GAD67.

conclusionsThese results suggest that ethanol induces hyper-differentiation of glutamatergic neuron through Pax6 pathway, which may underlie the hyper-excitability phenotype such as hyperactivity or seizure susceptibility in FASD patients.

Indexed as

Neural Stem CellsAnimalsCell DifferentiationCell ProliferationCells, CulturedEthanolEye ProteinsFemaleFetal Alcohol Spectrum Disordersgamma-Aminobutyric AcidGlutamic AcidHomeodomain ProteinsHumansMiceNeurogenesisNeuronsEthanolEye Proteinsgamma-Aminobutyric AcidGlutamic AcidHomeodomain ProteinsPaired Box Transcription FactorsPAX6 protein, humanPax6 protein, mousePax6 protein, ratPAX6 Transcription FactorRepressor Proteins

Identifiers

PMID21073715
PMCPMC2996361
OpenAlexW2070726583

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.