ArticleSchizophrenia research2013
Potential molecular mechanisms for decreased synaptic glutamate release in dysbindin-1 mutant mice.
Article in Schizophrenia research, 2013. 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, 30 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
- The Role of Dopamine D3 Receptors, Dysbindin, and Their Functional Interaction in the Expression of Key Genes for Neuroplasticity and Neuroinflammation in the Mouse Brain.International journal of molecular sciences · 2023Article
- Genetic Effects of the Schizophrenia-Related GeneFrontiers in genetics · 2021Article
- Loss of dysbindin-1 affects GABAergic transmission in the PFC.Psychopharmacology · 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
- Dysbindin-1 contributes to prefrontal cortical dendritic arbor pathology in schizophrenia.Schizophrenia research · 2018Article
- Neurodevelopmental disease mechanisms, primary cilia, and endosomes converge on the BLOC-1 and BORC complexes.Developmental neurobiology · 2018Review
- Dysbindin-1 Involvement in the Etiology of Schizophrenia.International journal of molecular sciences · 2017Review
- BLOC-1 deficiency causes alterations in amino acid profile and in phospholipid and adenosine metabolism in the postnatal mouse hippocampus.Scientific reports · 2017Article
- Effects of fingolimod administration in a genetic model of cognitive deficits.Journal of neuroscience research · 2017Article
- BDNF rescues prefrontal dysfunction elicited by pyramidal neuron-specific DTNBP1 deletion in vivo.Journal of molecular cell biology · 2017Article
- The Proteome of BLOC-1 Genetic Defects Identifies the Arp2/3 Actin Polymerization Complex to Function Downstream of the Schizophrenia Susceptibility Factor Dysbindin at the Synapse.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- The N-ethylmaleimide-sensitive factor and dysbindin interact to modulate synaptic plasticity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Mutations in the BLOC-1 subunits dysbindin and muted generate divergent and dosage-dependent phenotypes.The Journal of biological chemistry · 2014Article
- Alterations of the myristoylated, alanine-rich C kinase substrate (MARCKS) in prefrontal cortex in schizophrenia.Schizophrenia research · 2014Article
- Impairments in brain-derived neurotrophic factor-induced glutamate release in cultured cortical neurons derived from rats with intrauterine growth retardation: possible involvement of suppression of TrkB/phospholipase C-γ activation.Neurochemical research · 2014Article
- Dysbindin-1 loss compromises NMDAR-dependent synaptic plasticity and contextual fear conditioning.Hippocampus · 2014Article
- Synaptic plasticity, neural circuits, and the emerging role of altered short-term information processing in schizophrenia.Frontiers in synaptic neuroscience · 2014Review
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4 authors at 2 institutions in 1 country.
Funding
Abstract
Behavioral genetic studies of humans have associated variation in the DTNBP1 gene with schizophrenia and its cognitive deficit phenotypes. The protein encoded by DTNBP1, dysbindin-1, is expressed in forebrain neurons where it interacts with proteins mediating vesicular trafficking and exocytosis. It has been shown that loss of dysbindin-1 results in a decrease in glutamate release in the prefrontal cortex; however the mechanisms underlying this decrease are not fully understood. In order to investigate this question, we evaluated dysbindin-1 null mutant mice, using electrophysiological recordings of prefrontal cortical neurons, imaging studies of vesicles, calcium dynamics and Western blot measures of synaptic proteins and Ca(2+) channels. Dysbindin-1 null mice showed a decrease in the ready releasable pool of synaptic vesicles, decreases in quantal size, decreases in the probability of release and deficits in the rate of endo- and exocytosis compared with wild-type controls. Moreover, the dysbindin-1 null mice show decreases in the [Ca(2+)]i,expression of L- and N-type Ca(2+)channels and several proteins involved in synaptic vesicle trafficking and priming. Our results provide new insights into the mechanisms of action of dysbindin-1.
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