Evidence map›Paper›PMID 29449568›Full record

ArticleScientific reports2018

Binge Alcohol Exposure Causes Neurobehavioral Deficits and GSK3β Activation in the Hippocampus of Adolescent Rats.

Zhe Ji, Lin Yuan, Xiong Lu, Hanqing Ding, Jia Luo, Zun-Ji Ke

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. 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
2.2field-weighted citation impact, top 11% 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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  4. Longitudinal analysis of the ABCD® study.Developmental cognitive neuroscience · 2025
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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 3 institutions in 2 countries.

Zhe JiDepartment of Biochemistry, Shanghai University of Traditional Chinese Medicine, 1200 Cailun Road, Shanghai, 201203, China.
Lin YuanDepartment of Biochemistry, Shanghai University of Traditional Chinese Medicine, 1200 Cailun Road, Shanghai, 201203, China.
Xiong LuDepartment of Biochemistry, Shanghai University of Traditional Chinese Medicine, 1200 Cailun Road, Shanghai, 201203, China.
Hanqing DingDepartment of Biochemistry, Shanghai University of Traditional Chinese Medicine, 1200 Cailun Road, Shanghai, 201203, China.
Jia LuoDepartment of Biochemistry, Shanghai University of Traditional Chinese Medicine, 1200 Cailun Road, Shanghai, 201203, China. jialuo888@uky.edu.ORCID 0000-0002-6968-3618
Zun-Ji KeDepartment of Biochemistry, Shanghai University of Traditional Chinese Medicine, 1200 Cailun Road, Shanghai, 201203, China. kezunji@shutcm.edu.cn.ORCID 0000-0003-4038-2456
Shanghai University of Traditional Chinese Medicine · CNShanghai Jiao Tong University · CNUniversity of Kentucky · US

Funding

GSK3BETA, A MEDIATOR OF ETHANOL NEUROTOXICITYR01AA015407 · NIAAA · WEST VIRGINIA UNIVERSITY · PI JIA LUO · 2005 to 2026
$6.2M
ALCOHOL AND BREAST CANCERR01AA017226 · NIAAA · WEST VIRGINIA UNIVERSITY · PI LUO, JIA · 2008 to 2024
$5.2M
NIAAA NIH HHS R01 AA015407NIAAA NIH HHS R01 AA017226
6 · The paper itself

Abstract

Heavy alcohol exposure causes profound damage to the adolescent brain, particularly the hippocampus, which underlie some behavioral deficits. However, the underlying molecular mechanisms remain inconclusive. The current study sought to determine whether binge alcohol exposure affects the hippocampus-related behaviors and key signaling proteins that may mediate alcohol neurotoxicity in adolescent rats. Alcohol exposure reduced the number of both NeuN-positive and doublecortin-positive cells in the hippocampus. Alcohol also induced neurodegeneration which was confirmed by ultrastructural analysis by electronic microscopy and was accompanied with the activation of microglia. Binge alcohol exposure impaired spatial learning and memory which was evaluated by the Morris water maze. However, alcohol did not alter the spontaneous locomotor activity which was determined by the open field test. GSK3β is a multi-function serine/threonine protein kinase regulating both neuronal survival and neurogenesis and plays an important role in various neurodegenerative disorders. We have previously shown that GSK3β is a key mediator of alcohol-induced neuron apoptosis in the developing brain. We showed here binge alcohol exposure caused GSK3β activation by inducing dephosphorylation at Ser9 without affecting the phosphorylation of Tyr216 in the hippocampus. Thus, GSK3β may be involved in binge alcohol exposure-induced neuronal damage to the adolescent hippocampus.

Indexed as

AnimalsApoptosisBinge DrinkingBrainCell SurvivalDoublecortin ProteinFemaleGlycogen Synthase Kinase 3 betaHippocampusMaleMemoryNeurodegenerative DiseasesNeurogenesisNeuronsNeurotoxicity SyndromesRatsDcx protein, ratDoublecortin ProteinGlycogen Synthase Kinase 3 beta

Identifiers

PMID29449568
PMCPMC5814471
OpenAlexW2792063936

What OpenQuestion holds

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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.