ArticleThe Journal of biological chemistry2012
The cell adhesion molecule neuroplastin-65 is a novel interaction partner of γ-aminobutyric acid type A receptors.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 40 citations in OpenAlex.
- De novo variants in NPTN cause a neurodevelopmental disorder with autism and neuroplastin-PMCA hypofunction.Genome medicine · 2026Article
- Proteostasis regulation of GABABiomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025Review
- Neuroplastin exerts antiepileptic effects through binding to the α1 subunit of GABA type A receptors to inhibit the internalization of the receptors.Journal of translational medicine · 2023Article
- Neuroplastin 65 deficiency reduces amyloid plaque formation and cognitive deficits in an Alzheimer's disease mouse model.Frontiers in cellular neuroscience · 2023Article
- The Yin and Yang of GABAergic and Glutamatergic Synaptic Plasticity: Opposites in Balance by Crosstalking Mechanisms.Frontiers in synaptic neuroscience · 2022Review
- Neuroplastin in Neuropsychiatric Diseases.Genes · 2021Review
- Neuroplastin in human cognition: review of literature and future perspectives.Translational psychiatry · 2021Review
- Neuroplastin expression is essential for hearing and hair cell PMCA expression.Brain structure & function · 2021Article
- The amino-terminal domain of GluA1 mediates LTP maintenance via interaction with neuroplastin-65.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- The Immunoglobulin Superfamily Member Basigin Is Required for Complex Dendrite Formation inFrontiers in cellular neuroscience · 2021Article
- Retrograde Amnesia - A Question of Disturbed Calcium Levels?Frontiers in cellular neuroscience · 2021Review
- Clmp Regulates AMPA and Kainate Receptor Responses in the Neonatal Hippocampal CA3 and Kainate Seizure Susceptibility in Mice.Frontiers in synaptic neuroscience · 2020Article
- The Interaction of TRAF6 With Neuroplastin Promotes Spinogenesis During Early Neuronal Development.Frontiers in cell and developmental biology · 2020Article
- Essential role for InSyn1 in dystroglycan complex integrity and cognitive behaviors in mice.eLife · 2019Article
- Microarray Analysis of Gene Expression Changes in Neuroplastin 65-Knockout Mice: Implications for Abnormal Cognition and Emotional Disorders.Neuroscience bulletin · 2018Article
- GABA type a receptor trafficking and the architecture of synaptic inhibition.Developmental neurobiology · 2018Review
- Neuroplastin deletion in glutamatergic neurons impairs selective brain functions and calcium regulation: implication for cognitive deterioration.Scientific reports · 2017Article
- Increased Susceptibility to Ischemic Brain Injury in Neuroplastin 65-Deficient Mice Likely via Glutamate Excitotoxicity.Frontiers in cellular neuroscience · 2017Article
- δ Subunit-containing GABAA receptors are preferred targets for the centrally acting analgesic flupirtine.British journal of pharmacology · 2015Article
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
γ-Aminobutyric acid type A (GABA(A)) receptors are pentameric ligand-gated ion channels that mediate fast inhibition in the central nervous system. Depending on their subunit composition, these receptors exhibit distinct pharmacological properties and differ in their ability to interact with proteins involved in receptor anchoring at synaptic or extra-synaptic sites. Whereas GABA(A) receptors containing α1, α2, or α3 subunits are mainly located synaptically where they interact with the submembranous scaffolding protein gephyrin, receptors containing α5 subunits are predominantly found extra-synaptically and seem to interact with radixin for anchorage. Neuroplastin is a cell adhesion molecule of the immunoglobulin superfamily that is involved in hippocampal synaptic plasticity. Our results reveal that neuroplastin and GABA(A) receptors can be co-purified from rat brain and exhibit a direct physical interaction as demonstrated by co-precipitation and Förster resonance energy transfer (FRET) analysis in a heterologous expression system. The brain-specific isoform neuroplastin-65 co-localizes with GABA(A) receptors as shown in brain sections as well as in neuronal cultures, and such complexes can either contain gephyrin or be devoid of gephyrin. Neuroplastin-65 specifically co-localizes with α1 or α2 but not with α3 subunits at GABAergic synapses. In addition, neuroplastin-65 also co-localizes with GABA(A) receptor α5 subunits at extra-synaptic sites. Down-regulation of neuroplastin-65 by shRNA causes a loss of GABA(A) receptor α2 subunits at GABAergic synapses. These results suggest that neuroplastin-65 can co-localize with a subset of GABA(A) receptor subtypes and might contribute to anchoring and/or confining GABA(A) receptors to particular synaptic or extra-synaptic sites, thus affecting receptor mobility and synaptic strength.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.