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Updated: Jun 18, 2026
07:44
Evaluation of Synapse Density in Hippocampal Rodent Brain Slices
Published on: October 6, 2017
Dysbindin regulates hippocampal LTP by controlling NMDA receptor surface expression.
Tina Tze-Tsang Tang1, Feng Yang, Bo-Shiun Chen
1Receptor Biology Section, National Institute of Neurological Disorders and Stroke, Section on Neural Development and Plasticity, National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892-3714, USA.
Summary
Dysbindin, a gene linked to schizophrenia, controls NMDA receptor (NMDAR) surface levels. Loss of dysbindin increases NR2A subunits, enhancing synaptic plasticity and potentially impacting schizophrenia pathogenesis.
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- Abnormalities in N-methyl-D-aspartate receptor (NMDAR) function are linked to schizophrenia.
- Dysbindin is a schizophrenia-susceptibility gene expressed in the forebrain.
Purpose of the Study:
- To investigate the role of dysbindin in regulating NMDAR surface expression and function.
- To explore the impact of dysbindin on synaptic plasticity in the hippocampus.
Main Methods:
- Utilized imaging analyses and biotinylation experiments in dysbindin-null mutant mice.
- Measured NMDAR-mediated synaptic currents and long-term potentiation (LTP) in hippocampal neurons.
- Assessed the effect of exogenous dysbindin expression on NR2A surface levels.
Main Results:
- Dysbindin-null neurons showed increased surface expression of the NR2A subunit of NMDARs, but not NR2B.
- Disruption of dysbindin significantly enhanced NR2A-mediated synaptic currents and LTP in hippocampal slices.
- Exogenous dysbindin expression reduced NR2A surface expression.
Conclusions:
- Dysbindin selectively regulates the surface expression of the NR2A subunit of NMDARs.
- This regulation impacts hippocampal synaptic plasticity, specifically LTP.
- Dysbindin's role in NMDAR subunit regulation offers a novel link to schizophrenia pathophysiology.
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