ArticleNeurobiology of disease2010
Does gene deletion of AMPA GluA1 phenocopy features of schizoaffective disorder?
Article in Neurobiology of disease, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 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
43 citing papers in PubMed, 80 citations in OpenAlex.
- Article
- The GluA1 cytoplasmic tail regulates intracellular AMPA receptor trafficking and synaptic transmission onto dentate gyrus GABAergic interneurons, gating response to novelty.Molecular psychiatry · 2026Article
- The VGCC auxiliary subunit α2δ1 is an extracellular GluA1 interactor and regulates LTP, spatial memory, and seizure susceptibility.bioRxiv : the preprint server for biology · 2024Article
- Cacna1c deficiency in forebrain glutamatergic neurons alters behavior and hippocampal plasticity in female mice.Translational psychiatry · 2024Article
- Article
- Article
- Article
- Cerebellar glutamatergic system impacts spontaneous motor recovery by regulating Gria1 expression.NPJ Regenerative medicine · 2022Article
- Identification and functional evaluation of GRIA1 missense and truncation variants in individuals with ID: An emerging neurodevelopmental syndrome.American journal of human genetics · 2022Article
- Distinct contributions of GluA1-containing AMPA receptors of different hippocampal subfields to salience processing, memory and impulse control.Translational psychiatry · 2022Article
- Phenotyping Young GluA1 Deficient Mice - A Behavioral Characterization in a Genetic Loss-of-Function Model.Frontiers in behavioral neuroscience · 2022Article
- Comparative Severity Assessment of Genetic, Stress-Based, and Pharmacological Mouse Models of Depression.Frontiers in behavioral neuroscience · 2022Article
- Deletion of AMPA receptor GluA1 subunit gene (Gria1) causes circadian rhythm disruption and aberrant responses to environmental cues.Translational psychiatry · 2021Article
- Glutamatergic Dysfunction and Synaptic Ultrastructural Alterations in Schizophrenia and Autism Spectrum Disorder: Evidence from Human and Rodent Studies.International journal of molecular sciences · 2020Review
- Hippocampal-prefrontal coherence mediates working memory and selective attention at distinct frequency bands and provides a causal link between schizophrenia and its risk gene GRIA1.Translational psychiatry · 2019Article
- Stress-sensitive antidepressant-like effects of ketamine in the mouse forced swim test.PloS one · 2019Article
- Attenuation of Novelty-Induced Hyperactivity ofFrontiers in pharmacology · 2019Article
- Absent sleep EEG spindle activity in GluA1 (Gria1) knockout mice: relevance to neuropsychiatric disorders.Translational psychiatry · 2018Article
- Neurobiological Mechanisms of Stress Resilience and Implications for the Aged Population.Current neuropharmacology · 2018Review
- GluA1 AMPAR subunit deletion reduces the hedonic response to sucrose but leaves satiety and conditioned responses intact.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
16 authors at 6 institutions in 4 countries.
Funding
Abstract
Glutamatergic dysfunction is strongly implicated in schizophrenia and mood disorders. GluA1 knockout (KO) mice display schizophrenia- and depression-related abnormalities. Here, we asked whether GluA1 KO show mania-related abnormalities. KO were tested for behavior in approach/avoid conflict tests, responses to repeated forced swim exposure, and locomotor responses under stress and after psychostimulant treatment. The effects of rapid dopamine depletion and treatment with lithium or a GSK-3β inhibitor (SB216763) on KO locomotor hyperactivity were tested. Results showed that KO exhibited novelty- and stress-induced locomotor hyperactivity, reduced forced swim immobility and alterations in approach/avoid conflict tests. Psychostimulant treatment and dopamine depletion exacerbated KO locomotor hyperactivity. Lithium, but not SB216763, treatment normalized KO anxiety-related behavior and partially reversed hyperlocomotor behavior, and also reversed elevated prefrontal cortex levels of phospho-MARCKS and phospho-neuromodulin. Collectively, these findings demonstrate mania-related abnormalities in GluA1 KO and, combined with previous findings, suggest this mutant may provide a novel model of features of schizoaffective disorder.
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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.