ArticleMolecular and cellular neurosciences2014
The schizophrenia susceptibility gene DTNBP1 modulates AMPAR synaptic transmission and plasticity in the hippocampus of juvenile DBA/2J mice.
Article in Molecular and cellular neurosciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 25 citations in OpenAlex.
- Unravelling the genetic and molecular basis of low-frequency rTMS induced changes in functional connectivity density in schizophrenia patients with auditory verbal hallucinations.Translational psychiatry · 2025Article
- Synaptic mitochondria glycation contributes to mitochondrial stress and cognitive dysfunction.Brain : a journal of neurology · 2025Article
- The shallow cognitive map hypothesis: A hippocampal framework for thought disorder in schizophrenia.Schizophrenia (Heidelberg, Germany) · 2022Review
- Dysbindin-1 regulates mitochondrial fission and gamma oscillations.Molecular psychiatry · 2021Article
- The RNA-Binding Protein HuD Regulates Alternative Splicing and Alternative Polyadenylation in the Mouse Neocortex.Molecules (Basel, Switzerland) · 2021Article
- Genetic Effects of the Schizophrenia-Related GeneFrontiers in genetics · 2021Article
- Association of the Synapse-Associated Protein 97 (Frontiers in psychiatry · 2018Article
- Thorase variants are associated with defects in glutamatergic neurotransmission that can be rescued by Perampanel.Science translational medicine · 2017Article
- Emerging Synaptic Molecules as Candidates in the Etiology of Neurological Disorders.Neural plasticity · 2017Review
- 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
- Dissecting bipolar disorder complexity through epigenomic approach.Molecular psychiatry · 2016Review
- Time-dependent reversal of synaptic plasticity induced by physiological concentrations of oligomeric Aβ42: an early index of Alzheimer's disease.Scientific reports · 2016Article
- Dysbindin-1C is required for the survival of hilar mossy cells and the maturation of adult newborn neurons in dentate gyrus.The Journal of biological chemistry · 2014Article
- Notoginsenoside R1 increases neuronal excitability and ameliorates synaptic and memory dysfunction following amyloid elevation.Scientific reports · 2014Article
- The DNA methylome and transcriptome of different brain regions in schizophrenia and bipolar disorder.PloS one · 2014Article
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4 authors at 2 institutions in 1 country.
Funding
Abstract
The dystrobrevin binding protein (DTNBP) 1 gene has emerged over the last decade as a potential susceptibility locus for schizophrenia. While no causative mutations have been found, reduced expression of the encoded protein, dysbindin, was reported in patients. Dysbindin likely plays a role in the neuronal trafficking of proteins including receptors. One important pathway suspected to be affected in schizophrenia is the fast excitatory glutamatergic transmission mediated by AMPA receptors. Here, we investigated excitatory synaptic transmission and plasticity in hippocampal neurons from dysbindin-deficient sandy mice bred on the DBA/2J strain. In cultured neurons an enhancement of AMPAR responses was observed. The enhancement of AMPAR-mediated transmission was confirmed in hippocampal CA3-CA1 synapses, and was not associated with changes in the expression of GluA1-4 subunits or an increase in GluR2-lacking receptor complexes. Lastly, an enhancement in LTP was also found in these mice. These data provide compelling evidence that dysbindin, a widely suspected susceptibility protein in schizophrenia, is important for AMPAR-mediated synaptic transmission and plasticity in the developing hippocampus.
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