ArticleFrontiers in behavioral neuroscience2015
Loss of dysbindin-1, a risk gene for schizophrenia, leads to impaired group 1 metabotropic glutamate receptor function in mice.
Article in Frontiers in behavioral neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- Dysbindin-1 Mutation Alters Prefrontal Cortex Extracellular Glutamate and Dopamine In Vivo.International journal of molecular sciences · 2024Article
- Loss of dysbindin-1 in excitatory neurons in mice impacts NMDAR-dependent behaviors, neuronal morphology and synaptic transmission in the ventral hippocampus.Scientific reports · 2024Article
- Review
- Synaptic plasticity in schizophrenia pathophysiology.IBRO neuroscience reports · 2023Article
- Synaptic plasticity in schizophrenia pathophysiology.IBRO neuroscience reports · 2022Article
- Group 1 Metabotropic Glutamate Receptors in Neurological and Psychiatric Diseases: Mechanisms and Prospective.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2022Review
- Dysbindin-1, BDNF, and GABAergic Transmission in Schizophrenia.Frontiers in psychiatry · 2022Review
- Activating mGluBiological psychiatry · 2021Article
- Insights on the Functional Interaction between Group 1 Metabotropic Glutamate Receptors (mGluRI) and ErbB Receptors.International journal of molecular sciences · 2020Review
- In vivo glucose metabolism and glutamate levels in mGluR5 knockout mice: a multimodal neuroimaging study using [EJNMMI research · 2020Article
- Deletion of Dtnbp1 in mice impairs threat memory consolidation and is associated with enhanced inhibitory drive in the amygdala.Translational psychiatry · 2019Article
- Developmental Genes and Regulatory Proteins, Domains of Cognitive Impairment in Schizophrenia Spectrum Psychosis and Implications for Antipsychotic Drug Discovery: The Example of Dysbindin-1 Isoforms and Beyond.Frontiers in pharmacology · 2019Review
- Sleep/Wake Disruption in a Mouse Model of BLOC-1 Deficiency.Frontiers in neuroscience · 2018Article
- Article
- Role of mGluACS chemical neuroscience · 2017Article
- Dysbindin-1 Involvement in the Etiology of Schizophrenia.International journal of molecular sciences · 2017Review
- Review
- Drug Abuse and Psychosis: New Insights into Drug-induced Psychosis.Experimental neurobiology · 2017Review
- Gene × Environment Interactions in Schizophrenia: Evidence from Genetic Mouse Models.Neural plasticity · 2016Review
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Authors and funding
4 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
The expression of dysbindin-1, a protein coded by the risk gene dtnbp1, is reduced in the brains of schizophrenia patients. Evidence indicates a role of dysbindin-1 in dopaminergic and glutamatergic transmission. Glutamatergic transmission and plasticity at excitatory synapses is critically regulated by G-protein coupled metabotropic glutamate receptor (mGluR) family members, that have been implicated in schizophrenia. Here, we report a role of dysbindin-1 in hippocampal group 1 mGluR (mGluRI) function in mice. In hippocampal synaptoneurosomal preparations from sandy (sdy) mice, that have a loss of function mutation in dysbindin-1 gene, we observed a striking reduction in mGluRI agonist [(S)-3, 5-dihydroxyphenylglycine] (DHPG)-induced phosphorylation of extracellular signal regulated kinase 1/2 (ERK1/2). This mGluR-ERK1/2 deficit occurred in the absence of significant changes in protein levels of the two members of the mGluRI family (i.e., mGluR1 and mGluR5) or in another mGluRI signaling pathway, i.e., protein kinase C (PKC). Aberrant mGluRI-ERK1/2 signaling affected hippocampal synaptic plasticity in the sdy mutants as DHPG-induced long-term depression (LTD) at CA1 excitatory synapses was significantly reduced. Behavioral data suggest that the mGluRI hypofunction may underlie some of the cognitive abnormalities described in sdy mice as the administration of CDPPB (3-cyano-N-(1, 3-diphenyl-1H-pyrazol-5-yl benzamide), a positive allosteric modulator of mGluR5, rescued short-term object recognition and spatial learning and memory deficits in these mice. Taken together, our data suggest a novel role of dysbindin-1 in regulating mGluRI functions.
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