ArticleBiological psychiatry2011
Reduced dysbindin expression mediates N-methyl-D-aspartate receptor hypofunction and impaired working memory performance.
Article in Biological psychiatry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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Who cites it
65 citing papers in PubMed.
- An N-methyl-D-aspartate receptor agonist facilitates sleep-independent synaptic plasticity associated with working memory capacity enhancement.Scientific reports · 2011Trial
- 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 Use of Event-Related Potentials in the Study of Schizophrenia: An Overview.Advances in neurobiology · 2024Review
- N-methyl-D-aspartate receptor hypofunction as a potential contributor to the progression and manifestation of many neurological disorders.Frontiers in molecular neuroscience · 2023Review
- Advantages and Limitations of Animal Schizophrenia Models.International journal of molecular sciences · 2022Review
- What Can We Learn from Animal Models to Study Schizophrenia?Advances in experimental medicine and biology · 2022Article
- Schizophrenia-associated dysbindin modulates axonal mitochondrial movement in cooperation with p150Molecular brain · 2021Article
- A Selective Review of the Excitatory-Inhibitory Imbalance in Schizophrenia: Underlying Biology, Genetics, Microcircuits, and Symptoms.Frontiers in cell and developmental biology · 2021Review
- In Vitro and In Vivo Models for the Investigation of Potential Drugs Against Schizophrenia.Biomolecules · 2020Review
- The origin of NMDA receptor hypofunction in schizophrenia.Pharmacology & therapeutics · 2020Review
- Loss of dysbindin-1 affects GABAergic transmission in the PFC.Psychopharmacology · 2019Article
- Deletion of Dtnbp1 in mice impairs threat memory consolidation and is associated with enhanced inhibitory drive in the amygdala.Translational psychiatry · 2019Article
- The gut microbiome from patients with schizophrenia modulates the glutamate-glutamine-GABA cycle and schizophrenia-relevant behaviors in mice.Science advances · 2019Article
- Can N-Methyl-D-Aspartate Receptor Hypofunction in Schizophrenia Be Localized to an Individual Cell Type?Frontiers in psychiatry · 2019Review
- An Overview of Animal Models Related to Schizophrenia.Canadian journal of psychiatry. Revue canadienne de psychiatrie · 2019Review
- Dysbindin-1 contributes to prefrontal cortical dendritic arbor pathology in schizophrenia.Schizophrenia research · 2018Article
- Effect of NMDA on proliferation and apoptosis in hippocampal neural stem cells treated with MK-801.Experimental and therapeutic medicine · 2018Article
- Bidirectional variation in glutamate efflux in the medial prefrontal cortex induced by selective positive and negative allosteric mGluR5 modulators.Journal of neurochemistry · 2018Article
- Salivary biomarkers for the diagnosis and monitoring of neurological diseases.Biomedical journal · 2018Review
5 more citing papers are in PubMed but not listed here.
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7 authors.
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Abstract
backgroundSchizophrenia is a heritable disorder associated with disrupted neural transmission and dysfunction of brain systems involved in higher cognition. The gene encoding dystrobrevin-binding-protein-1 (dysbindin) is a putative candidate gene associated with cognitive impairments, including memory deficits, in both schizophrenia patients and unaffected individuals. The underlying mechanism is thought to be based in changes in glutamatergic and dopaminergic function within the corticostriatal networks known to be critical for schizophrenia. This hypothesis derives support from studies of mice with a null mutation in the dysbindin gene that exhibit memory dysfunction and excitatory neurotransmission abnormalities in prefrontal and hippocampal networks. At a cellular level, dysbindin is thought to mediate presynaptic glutamatergic transmission.
methodsWe investigated the relationship between glutamate receptor dynamics and memory performance in dysbindin mutant mice. We assessed N-methyl-D-aspartate (NMDA) and α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor function in prefrontal cortex pyramidal neurons in vitro with whole-cell recordings, molecular quantitative analyses (reverse transcription-polymerase chain reaction) of the mandatory NMDA receptor subunit NR1, and cognitive function with a spatial working memory task.
resultsDecreases in dysbindin are associated with specific decreases in NMDA-evoked currents in prefrontal pyramidal neurons, as well as decreases in NR1 expression. Furthermore, the degree of NR1 expression correlates with spatial working memory performance, providing a mechanistic explanation for cognitive changes previously associated with dysbindin expression.
conclusionsThese data show a significant downregulation of NMDA receptors due to dysbindin deficiency and illuminate molecular mechanisms mediating the association between dysbindin insufficiency and cognitive impairments associated with schizophrenia, encouraging study of the dysbindin/NR1 expression association in humans with schizophrenia.
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