Evidence map›Paper›PMID 35589394›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2022

Oxidative Stress-Induced Damage to the Developing Hippocampus Is Mediated by GSK3β.

Joseph Abbah, Claire-Marie Vacher, Evan Z Goldstein, Zhen Li, Srikanya Kundu, Brooke Talbot, Surajit Bhattacharya, Kazue Hashimoto-Torii, Li Wang, Payal Banerjee and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
13.7field-weighted citation impact, top 1% 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

23 citing papers in PubMed, 37 citations in OpenAlex.

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  17. IL-6 Enhances the Activation of PI3K-AKT/mTOR-GSK-3β by Upregulating GRPR in Hippocampal Neurons of Autistic Mice.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2024
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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

14 authors at 1 institution in 1 country.

Joseph AbbahCenter for Neuroscience Research, Children's National Research Institute, Children's National Hospital, Washington, DC 20010.
Claire-Marie VacherCenter for Neuroscience Research, Children's National Research Institute, Children's National Hospital, Washington, DC 20010.
Evan Z GoldsteinCenter for Neuroscience Research, Children's National Research Institute, Children's National Hospital, Washington, DC 20010 VGallo@childrensnational.org egoldstein@childrensnational.org.
Zhen LiCenter for Neuroscience Research, Children's National Research Institute, Children's National Hospital, Washington, DC 20010.
Srikanya KunduCenter for Neuroscience Research, Children's National Research Institute, Children's National Hospital, Washington, DC 20010.
Brooke TalbotCenter for Neuroscience Research, Children's National Research Institute, Children's National Hospital, Washington, DC 20010.
Surajit BhattacharyaCenter for Genetic Medicine, Children's National Research Institute, Children's National Hospital, Washington, DC 20010.
Kazue Hashimoto-ToriiCenter for Neuroscience Research, Children's National Research Institute, Children's National Hospital, Washington, DC 20010.
Li WangCenter for Neuroscience Research, Children's National Research Institute, Children's National Hospital, Washington, DC 20010.
Payal BanerjeeBioinformatics Core, Children's National Research Institute, Children's National Hospital, Washington, DC 20010.
Joseph ScafidiCenter for Neuroscience Research, Children's National Research Institute, Children's National Hospital, Washington, DC 20010.
Nathan A SmithCenter for Neuroscience Research, Children's National Research Institute, Children's National Hospital, Washington, DC 20010.ORCID https://orcid.org/0000-0002-9254-5360
Li-Jin ChewCenter for Neuroscience Research, Children's National Research Institute, Children's National Hospital, Washington, DC 20010.
Vittorio GalloCenter for Neuroscience Research, Children's National Research Institute, Children's National Hospital, Washington, DC 20010 VGallo@childrensnational.org egoldstein@childrensnational.org.
Children's National · US

Funding

Neurobehavioral Evaluation CoreP50HD105328 · NICHD · CHILDREN'S RESEARCH INSTITUTE · PI LAUREN KENWORTHY · 2021 to 2026
$9.3M
Research_ProjectU54HD090257 · NICHD · CHILDREN'S RESEARCH INSTITUTE · PI GUAY-WOODFORD, LISA MARIE · 2016 to 2020
$5.9M
Mechanisms of Oligodendrocyte and Axonal Abnormalities After Perinatal Brain InjuryR37NS109478 · NINDS · SEATTLE CHILDREN'S HOSPITAL · PI GALLO, VITTORIO · 2018 to 2025
$3.1M
Astrocytes Modulate Synaptic Plasticity via NorepinephrineK01NS110981 · NINDS · UNIVERSITY OF ROCHESTER · PI SMITH, NATHAN A · 2019 to 2024
$1.1M
Functional mechanisms underlying hippocampal damage and behavioral abnormalities caused by perinatal hyperoxiaR21NS095351 · NINDS · CHILDREN'S RESEARCH INSTITUTE · PI VITTORIO GALLO, VITTORIO GALLO VITTORIO GALLO · 2016 to 2017
$481k
NICHD NIH HHS P50 HD105328NICHD NIH HHS U54 HD090257NINDS NIH HHS K01 NS110981NINDS NIH HHS R21 NS095351NINDS NIH HHS R37 NS109478
6 · The paper itself

Abstract

Neonatal brain injury renders the developing brain vulnerable to oxidative stress, leading to cognitive deficit. However, oxidative stress-induced damage to hippocampal circuits and the mechanisms underlying long-term changes in memory and learning are poorly understood. We used high oxygen tension or hyperoxia (HO) in neonatal mice of both sexes to investigate the role of oxidative stress in hippocampal damage. Perinatal HO induces reactive oxygen species and cell death, together with reduced interneuron maturation, inhibitory postsynaptic currents, and dentate progenitor proliferation. Postinjury interneuron stimulation surprisingly improved inhibitory activity and memory tasks, indicating reversibility. With decreased hippocampal levels of Wnt signaling components and somatostatin, HO aberrantly activated glycogen synthase kinase 3 β activity. Pharmacological inhibition or ablation of interneuron glycogen synthase kinase 3 β during HO challenge restored progenitor cell proliferation, interneuron development, inhibitory/excitatory balance, as well as hippocampal-dependent behavior. Biochemical targeting of interneuron function may benefit learning deficits caused by oxidative damage.

Indexed as

Brain InjuriesHyperoxiaOxidative StressAnimalsFemaleGlycogen Synthase Kinase 3 betaHippocampusHumansMaleMiceOxygenPregnancyGlycogen Synthase Kinase 3 betaGsk3b protein, mouseOxygenAktexcitation–inhibition balanceGABAinterneuronsmemoryPOMC

Identifiers

PMID35589394
PMCPMC9188427
OpenAlexW4281261003

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.