Evidence map›Paper›PMID 27371763›Full record

ArticleCerebral cortex (New York, N.Y. : 1991)2017

Developmental Alcohol Exposure Impairs Activity-Dependent S-Nitrosylation of NDEL1 for Neuronal Maturation.

Atsushi Saito, Yu Taniguchi, Sun-Hong Kim, Balakrishnan Selvakumar, Gabriel Perez, Michael D Ballinger, Xiaolei Zhu, James Sabra, Mariama Jallow, Priscilla Yan and 7 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cerebral cortex (New York, N.Y. : 1991), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

7 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
  2. Article
  3. Behavioral Deficits in Mice with Postnatal Disruption ofCerebral cortex communications · 2021
    Article
  4. Article
  5. Article
  6. Adolescent ΔBiological psychiatry · 2019
    Article
  7. Review
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

17 authors at 5 institutions in 2 countries.

Atsushi SaitoDepartment of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Yu TaniguchiDepartment of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Sun-Hong KimDepartment of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Balakrishnan SelvakumarDepartment of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Gabriel PerezDepartment of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Michael D BallingerDepartment of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Xiaolei ZhuDepartment of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
James SabraDepartment of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Mariama JallowDepartment of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Priscilla YanDepartment of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Koki ItoDepartment of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Shreenath RajendranDepartment of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Shinji HirotsuneDepartment of Genetic Disease Research, Osaka City University Graduate School of Medicine, Abeno, Osaka 545-8585, Japan.
Anthony Wynshaw-BorisDepartment of Genetics and Genome Sciences, Case Western Reserve University, Cleveland, OH 44106, USA.
Solomon H SnyderDepartment of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Akira SawaDepartment of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Atsushi KamiyaDepartment of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Johns Hopkins Medicine · USJohns Hopkins University · USCase Western Reserve University · USDokkyo Medical University · JPOsaka City University · JP

Funding

Project 3P50MH094268 · NIMH · JOHNS HOPKINS UNIVERSITY · PI SAWA, AKIRA · 2011 to 2020
$19.9M
DISC1 Pathway in Dendritogenesis: Implications for Dopamine Circuit and CognitionR01MH091230 · NIMH · JOHNS HOPKINS UNIVERSITY · PI KAMIYA, ATSUSHI · 2010 to 2014
$1.6M
Exploring depressive behavior using a natural product for novel drug targetsR21AT008547 · NCCIH · JOHNS HOPKINS UNIVERSITY · PI KAMIYA, ATSUSHI · 2014 to 2015
$439k
NCCIH NIH HHS R21 AT008547NIMH NIH HHS P50 MH094268NIMH NIH HHS R01 MH091230
6 · The paper itself

Abstract

Neuronal nitric oxide synthase is involved in diverse signaling cascades that regulate neuronal development and functions via S-Nitrosylation-mediated mechanism or the soluble guanylate cyclase (sGC)/cyclic guanosine monophosphate (cGMP) pathway activated by nitric oxide. Although it has been studied extensively in vitro and in invertebrate animals, effects on mammalian brain development and underlying mechanisms remain poorly understood. Here we report that genetic deletion of "Nos1" disrupts dendritic development, whereas pharmacological inhibition of the sGC/cGMP pathway does not alter dendritic growth during cerebral cortex development. Instead, nuclear distribution element-like (NDEL1), a protein that regulates dendritic development, is specifically S-nitrosylated at cysteine 203, thereby accelerating dendritic arborization. This post-translational modification is enhanced by N-methyl-D-aspartate receptor-mediated neuronal activity, the main regulator of dendritic formation. Notably, we found that disruption of S-Nitrosylation of NDEL1 mediates impaired dendritic maturation caused by developmental alcohol exposure, a model of developmental brain abnormalities resulting from maternal alcohol use. These results highlight S-Nitrosylation as a key activity-dependent mechanism underlying neonatal brain maturation and suggest that reduction of S-Nitrosylation of NDEL1 acts as a pathological factor mediating neurodevelopmental abnormalities caused by maternal alcohol exposure.

Indexed as

AnimalsCarrier ProteinsDendritesDisease Models, AnimalFetal Alcohol Spectrum DisordersHumansMice, Inbred C57BLMice, TransgenicMutationNitric Oxide Synthase Type IPrefrontal CortexPyramidal CellsSynaptic TransmissionCarrier ProteinsNDEL1 protein, humanNdel1 protein, mouseNitric Oxide Synthase Type INos1 protein, mousedendritic developmentfetal alcohol spectrum disorderNDEL1neuronal activityS-Nitrosylation

Identifiers

PMID27371763
PMCPMC6248727
OpenAlexW2464040546

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.