ArticleGenes2016
Imbalance between Glutamate and GABA in Fmr1 Knockout Astrocytes Influences Neuronal Development.
Article in Genes, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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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.
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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
14 citing papers in PubMed, 27 citations in OpenAlex.
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- Exploring the Mechanism of 2'-Hydroxychalcone Improving Copper Sulfate-Induced Inflammation in Zebrafish Through Network Pharmacology.Drug design, development and therapy · 2025Article
- Unlocking Neural Function with 3D In Vitro Models: A Technical Review of Self-Assembled, Guided, and Bioprinted Brain Organoids and Their Applications in the Study of Neurodevelopmental and Neurodegenerative Disorders.International journal of molecular sciences · 2023Review
- Adolescent intermittent ethanol exposure enhances adult stress effects in male rats.Pharmacology, biochemistry, and behavior · 2023Article
- Garden Cress (Neuropsychiatric disease and treatment · 2023Article
- Longitudinal PET studies of mGluR5 in FXS using an FMR1 knockout mouse model.Translational neuroscience · 2022Article
- Astrocyte: A Foe or a Friend in Intellectual Disability-Related Diseases.Frontiers in synaptic neuroscience · 2022Review
- Spermine protects aluminium chloride and iron-induced neurotoxicity in rat model of Alzheimer's disease via attenuation of tau phosphorylation, Amyloid-β (1-42) and NF-κB pathway.Inflammopharmacology · 2021Article
- Allicin ameliorates aluminium- and copper-induced cognitive dysfunction in Wistar rats: relevance to neuro-inflammation, neurotransmitters and AβJournal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2021Article
- Disrupted Association of Sensory Neurons With Enveloping Satellite Glial Cells in Fragile X Mouse Model.Frontiers in molecular neuroscience · 2021Article
- Tea polyphenols protect learning and memory in sleep-deprived mice by promoting AMPA receptor internalization.Neuroreport · 2020Article
- NDRG2 Protects the Brain from Excitotoxicity by Facilitating Interstitial Glutamate Uptake.Translational stroke research · 2020Article
- Molecular Biomarkers in Fragile X Syndrome.Brain sciences · 2019Review
- Postsynaptic FMRP Regulates SynaptogenesisThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fragile X syndrome (FXS) is a form of inherited mental retardation that results from the absence of the fragile X mental retardation protein (FMRP), the product of the Fmr1 gene. Numerous studies have shown that FMRP expression in astrocytes is important in the development of FXS. Although astrocytes affect neuronal dendrite development in Fmr1 knockout (KO) mice, the factors released by astrocytes are still unclear. We cultured wild type (WT) cortical neurons in astrocyte-conditioned medium (ACM) from WT or Fmr1 KO mice. Immunocytochemistry and Western blotting were performed to detect the dendritic growth of both WT and KO neurons. We determined glutamate and γ-aminobutyric acid (GABA) levels using high-performance liquid chromatography (HPLC). The total neuronal dendritic length was reduced when cultured in the Fmr1 KO ACM. This neurotoxicity was triggered by an imbalanced release of glutamate and GABA from Fmr1 KO astrocytes. We found increased glutaminase and GABA transaminase (GABA-T) expression and decreased monoamine oxidase B expression in Fmr1 KO astrocytes. The elevated levels of glutamate contributed to oxidative stress in the cultured neurons. Vigabatrin (VGB), a GABA-T inhibitor, reversed the changes caused by glutamate and GABA release in Fmr1 KO astrocytes and the abnormal behaviors in Fmr1 KO mice. Our results indicate that the imbalance in the astrocytic glutamate and GABA release may be involved in the neuropathology and the underlying symptoms of FXS, and provides a therapeutic target for treatment.
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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.