Evidence map›Paper›PMID 33482226›Full record

ArticleExperimental neurology2021

Adult glut3 homozygous null mice survive to demonstrate neural excitability and altered neurobehavioral responses reminiscent of neurodevelopmental disorders.

Bo-Chul Shin, Carlos Cepeda, Mason Eghbali, Shin Yun Byun, Michael S Levine, Sherin U Devaskar

Open access · greenAbstract read
In one paragraph

Article in Experimental neurology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.5field-weighted citation impact, top 31% 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

8 citing papers in PubMed, 9 citations in OpenAlex.

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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

6 authors at 1 institution in 1 country.

Bo-Chul ShinDepartments of Pediatrics, Division of Neonatology & Developmental Biology, The Neonatal Research Center of the UCLA Children's Discovery & Innovation Institute, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095-1752, United States of America.
Carlos CepedaIntellectual and Developmental Disabilities Research Center and Brain Research Institute, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095-1752, United States of America.
Mason EghbaliDepartments of Pediatrics, Division of Neonatology & Developmental Biology, The Neonatal Research Center of the UCLA Children's Discovery & Innovation Institute, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095-1752, United States of America.
Shin Yun ByunDepartments of Pediatrics, Division of Neonatology & Developmental Biology, The Neonatal Research Center of the UCLA Children's Discovery & Innovation Institute, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095-1752, United States of America.
Michael S LevineIntellectual and Developmental Disabilities Research Center and Brain Research Institute, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095-1752, United States of America.
Sherin U DevaskarDepartments of Pediatrics, Division of Neonatology & Developmental Biology, The Neonatal Research Center of the UCLA Children's Discovery & Innovation Institute, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095-1752, United States of America. Electronic address: Sdevaskar@mednet.ucla.edu.
UCLA Health · US

Funding

UCLA IDDRC: Translational CoreP50HD103557 · NICHD · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SUSAN Y BOOKHEIMER · 2020 to 2026
$9.6M
Prenatal Metabolic Programming of the OffspringR01HD041230 · NICHD · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DEVASKAR, SHERIN U · 2001 to 2019
$5.2M
Prenatal Origins of Neurometabolic ConsequencesR01HD081206 · NICHD · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DEVASKAR, SHERIN U · 2015 to 2024
$4.1M
NICHD NIH HHS P50 HD103557NICHD NIH HHS R01 HD041230NICHD NIH HHS R01 HD081206
6 · The paper itself

Abstract

Since GLUT3 is vital for fueling neurotransmission, we examined in-vivo the adult phenotype carrying the conditional homozygous glut3 gene mutation (KO) in glutamate-excitatory neurons. These KO mice demonstrated sex-specific differences in brain and body weights (p = 0.0001 and p = 0.01 each) with reduced GLUT3 protein in cerebral cortices and brain stem (p = 0.005). In patch clamp studies the glut3 KO mice displayed a shorter latency to and enhanced paroxysmal activity (p = 0.01 and p = 0.015 each) in pyramidal neurons upon application of a GABA

Indexed as

AnimalsBehavior, AnimalBrainDisease Models, AnimalFemaleGlucose Transporter Type 3MaleMiceMice, Inbred C57BLMice, KnockoutNeurodevelopmental DisordersPyramidal CellsGlucose Transporter Type 3Glutamate-excitatory neuronsLoss-of-function polymorphismsNeurodevelopmental disordersSeizure activity

Identifiers

PMID33482226
PMCPMC8281499
OpenAlexW3121397823

What OpenQuestion holds

Textmetadata
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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.