ArticleAlcoholism, clinical and experimental research2017
Prenatal Alcohol Exposure Leads to Enhanced Serine 9 Phosphorylation of Glycogen Synthase Kinase-3β (GSK-3β) in the Hippocampal Dentate Gyrus of Adult Mouse.
Article in Alcoholism, clinical and experimental research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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.
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.
Who cites it
7 citing papers in PubMed, 16 citations in OpenAlex.
- New insights into the role of GSK-3β in the brain: from neurodegenerative disease to tumorigenesis.PeerJ · 2023Review
- Corticostriatal Circuit Models of Cognitive Impairments Induced by Fetal Exposure to Alcohol.Biological psychiatry · 2021Review
- Pre-implantation alcohol exposure induces lasting sex-specific DNA methylation programming errors in the developing forebrain.Clinical epigenetics · 2021Article
- Functional and Structural Correlates of Impaired Enrichment-Mediated Adult Hippocampal Neurogenesis in a Mouse Model of Prenatal Alcohol Exposure.Brain plasticity (Amsterdam, Netherlands) · 2020Article
- Pharmacological inhibition of glycogen synthase kinase 3 increases operant alcohol self-administration in a manner associated with altered pGSK-3β, protein interacting with C kinase and GluA2 protein expression in the reward pathway of male C57BL/6J mice.Behavioural pharmacology · 2020Article
- Resistance of Postnatal Hippocampal Neurogenesis to Alcohol Toxicity in a Third Trimester-Equivalent Mouse Model of Gestational Alcohol Exposure.Alcoholism, clinical and experimental research · 2019Article
- Alcohol drinking exacerbates neural and behavioral pathology in the 3xTg-AD mouse model of Alzheimer's disease.International review of neurobiology · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe goal of this study was to evaluate the expression and serine 9 phosphorylation of glycogen synthase kinase (GSK-3β) within the adult hippocampal dentate gyrus (DG) in a preclinical mouse model of fetal alcohol spectrum disorders. GSK-3β is a multifunctional kinase that modulates many hippocampal processes affected by gestational alcohol, including synaptic plasticity and adult neurogenesis. GSK-3β is a constitutively active kinase that is negatively regulated by phosphorylation at the serine 9 residue.
methodsWe utilized a well-characterized limited access "drinking-in-the-dark" paradigm of prenatal alcohol exposure (PAE) and measured p(Ser9)GSK-3β and total GSK-3β within adult DG by Western blot analysis. In addition, we evaluated the expression pattern of both p(Ser9)GSK-3β and total GSK-3β within the adult hippocampal dentate of PAE and control mice using high-resolution confocal microscopy.
resultsOur findings demonstrate a marked 2.0-fold elevation of p(Ser9)GSK-3β in PAE mice, concomitant with a more moderate 36% increase in total GSK-3β. This resulted in an approximate 63% increase in the p(Ser9)GSK-3β/GSK-3β ratio. Immunostaining revealed robust GSK-3β expression within Cornu Ammonis (CA) pyramidal neurons, hilar mossy cells, and a subset of GABAergic interneurons, with low levels of expression within hippocampal progenitors and dentate granule cells.
conclusionsThese findings suggest that PAE may lead to a long-term disruption of GSK-3β signaling within the DG, and implicate mossy cells, GABAergic interneurons, and CA primary neurons as major targets of this dysregulation.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.