ArticleBiological research2017
Neurochemical and behavioral characterization of neuronal glutamate transporter EAAT3 heterozygous mice.
Article in Biological research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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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Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
- Advancing Obsessive-Compulsive Disorder Research: Insights from Transgenic Animal Models and Innovative Therapies.Brain sciences · 2025Review
- Neurobiology of Obsessive-Compulsive Disorder from Genes to Circuits: Insights from Animal Models.Neuroscience bulletin · 2024Review
- Article
- Developmental impact of glutamate transporter overexpression on dopaminergic neuron activity and stereotypic behavior.Molecular psychiatry · 2022Article
- Altered Grooming Syntax and Amphetamine-Induced Dopamine Release in EAAT3 Overexpressing Mice.Frontiers in cellular neuroscience · 2021Article
- Animal Models for OCD Research.Current topics in behavioral neurosciences · 2021Review
- Behavioral and synaptic alterations relevant to obsessive-compulsive disorder in mice with increased EAAT3 expression.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2019Article
- Neuronal excitatory amino acid transporter EAAT3: Emerging functions in health and disease.Neurochemistry international · 2019Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundObsessive-compulsive disorder (OCD) is a severe neuropsychiatric condition affecting 1-3% of the worldwide population. OCD has a strong genetic component, and the SLC1A1 gene that encodes neuronal glutamate transporter EAAT3 is a strong candidate for this disorder. To evaluate the impact of reduced EAAT3 expression in vivo, we studied male EAAT3 heterozygous and wild-type littermate mice using a battery of behavioral paradigms relevant to anxiety (open field test, elevated plus maze) and compulsivity (marble burying), as well as locomotor activity induced by amphetamine. Using high-performance liquid chromatography, we also determined tissue neurotransmitter levels in cortex, striatum and thalamus-brain areas that are relevant to OCD.
resultsCompared to wild-type littermates, EAAT3 heterozygous male mice have unaltered baseline anxiety-like, compulsive-like behavior and locomotor activity. Administration of acute amphetamine (5 mg/kg intraperitoneally) increased locomotion with no differences across genotypes. Tissue levels of glutamate, GABA, dopamine and serotonin did not vary between EAAT3 heterozygous and wild-type mice.
conclusionsOur results indicate that reduced EAAT3 expression does not impact neurotransmitter content in the corticostriatal circuit nor alter anxiety or compulsive-like behaviors.
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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.