Evidence map›Paper›PMID 24746641›Full record

ArticleNeurotoxicology and teratology

Ketamine exposure in early development impairs specification of the primary germ cell layers.

Oluwaseun Akeju, Brandi N Davis-Dusenbery, Seth H Cassel, Justin K Ichida, Kevin Eggan

Open access · greenAbstract read
In one paragraph

Article in Neurotoxicology and teratology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

5 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Evaluating the control: minipump implantation and breathing behavior in the neonatal rat.Journal of applied physiology (Bethesda, Md. : 1985) · 2016
    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 1 country.

Oluwaseun AkejuDepartment of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA; The Howard Hughes Medical Institute, Harvard Stem Cell Institute, Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA 02138, USA. Electronic address: oluwaseun.akeju@mgh.harvard.edu.
Brandi N Davis-DusenberyThe Howard Hughes Medical Institute, Harvard Stem Cell Institute, Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA 02138, USA.
Seth H CasselThe Howard Hughes Medical Institute, Harvard Stem Cell Institute, Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA 02138, USA.
Justin K IchidaThe Howard Hughes Medical Institute, Harvard Stem Cell Institute, Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA 02138, USA.
Kevin EgganThe Howard Hughes Medical Institute, Harvard Stem Cell Institute, Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA 02138, USA.
Harvard Stem Cell Institute · USHoward Hughes Medical Institute · US

Funding

Research Training for AnesthetistsT32GM007592 · NIGMS · MASSACHUSETTS GENERAL HOSPITAL · PI STUART A FORMAN · 1985 to 2026
$11.8M
Conversion of Fibroblasts to fxnal Spinal Motor Neurons Using Defined FactorR00NS077435 · NINDS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI ICHIDA, JUSTIN KAWIKA · 2013 to 2015
$737k
Howard Hughes Medical InstituteNIGMS NIH HHS T32 GM007592NIGMS NIH HHS T32GM007592NINDS NIH HHS R00 NS077435
6 · The paper itself

Abstract

Preclinical and clinical evidence implicates N-methyl-d-aspartate receptor (NMDAr) signaling in early embryological development. However, the role of NMDAr signaling in early development has not been well studied. Here, we use a mouse embryonic stem cell model to perform a step-wise exploration of the effects of NMDAr signaling on early cell fate specification. We found that antagonism of the NMDAr impaired specification into the neuroectodermal and mesoendodermal cell lineages, with little or no effect on specification of the extraembryonic endoderm cell lineage. Consistent with these findings, exogenous NMDA promoted neuroectodermal differentiation. Finally, NMDAr antagonism modified expression of several key targets of TGF-β superfamily signaling, suggesting a mechanism for these findings. In summary, this study shows that NMDAr antagonism interferes with the normal developmental pathways of embryogenesis, and suggests that interference is most pronounced prior to neuroectodermal and mesoendodermal cell fate specification.

Indexed as

AnimalsCell DifferentiationDevelopmental DisabilitiesDizocilpine MaleateDose-Response Relationship, DrugEmbryoid BodiesEmbryo, MammalianEmbryonic DevelopmentExcitatory Amino Acid AntagonistsFemaleFlow CytometryKetamineMaleMiceMicroarray AnalysisMotor NeuronsDizocilpine MaleateExcitatory Amino Acid AntagonistsKetamineNerve Tissue ProteinsDifferentiationKetamineMesoendodermMouse embryonic stem cellsNeurogenesisNMDA

Identifiers

PMID24746641
PMCPMC4046705
OpenAlexW2037221007

What OpenQuestion holds

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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.