ArticleJournal of translational medicine2023
Neuroplastin exerts antiepileptic effects through binding to the α1 subunit of GABA type A receptors to inhibit the internalization of the receptors.
Article in Journal of translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 16 citations in OpenAlex.
- GABASynapse (New York, N.Y.) · 2026Review
- AAV-mediated GPR173 gene therapy attenuates long-term refractory epilepsy by enhancing synaptic GABAActa pharmacologica Sinica · 2026Article
- De novo variants in NPTN cause a neurodevelopmental disorder with autism and neuroplastin-PMCA hypofunction.Genome medicine · 2026Article
- Pantothenic Acid Protects Neurons After Ischemic Stroke by Targeting ID3 to Restore Action Potential Amplitude.Journal of neuroscience research · 2026Article
- Identification and quantification of GABAIBRO neuroscience reports · 2025Article
- The Role of HIF-1α/BNIP3 Pathway in Hippocampal Neuronal Autophagy in Epilepsy.Molecular neurobiology · 2025Article
- Causal relations of trace elements and nutrients with insomnia: A Mendelian randomization study.Medicine · 2025Article
- Elevated Release of Presynaptic Glutamate: The Potential Pathogenesis of Anti-NMDAR Encephalitis-Associated Seizures.CNS neuroscience & therapeutics · 2025Article
- Rab11a-dependent recycling of Glut3 inhibits seizure-induced neuronal disulfidptosis by alleviating glucose deficiency.Cell & bioscience · 2025Article
- Proteostasis regulation of GABABiomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025Review
- GluN2B influences the progression of status epilepticus by modulating calcium ion homeostasis through its interaction with CaMKIIα.Frontiers in pharmacology · 2025Article
- Technological Vanguard: the outstanding performance of the LTY-CNN model for the early prediction of epileptic seizures.Journal of translational medicine · 2024Article
- NDUFA11 may be the disulfidptosis-related biomarker of ischemic stroke based on integrated bioinformatics, clinical samples, and experimental analyses.Frontiers in neuroscience · 2024Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSeizures are associated with a decrease in γ-aminobutyric type A acid receptors (GABAaRs) on the neuronal surface, which may be regulated by enhanced internalization of GABAaRs. When interactions between GABAaR subunit α-1 (GABRA1) and postsynaptic scaffold proteins are weakened, the α1-containing GABAaRs leave the postsynaptic membrane and are internalized. Previous evidence suggested that neuroplastin (NPTN) promotes the localization of GABRA1 on the postsynaptic membrane. However, the association between NPTN and GABRA1 in seizures and its effect on the internalization of α1-containing GABAaRs on the neuronal surface has not been studied before.
methodsAn in vitro seizure model was constructed using magnesium-free extracellular fluid, and an in vivo model of status epilepticus (SE) was constructed using pentylenetetrazole (PTZ). Additionally, in vitro and in vivo NPTN-overexpression models were constructed. Electrophysiological recordings and internalization assays were performed to evaluate the action potentials and miniature inhibitory postsynaptic currents of neurons, as well as the intracellular accumulation ratio of α1-containing GABAaRs in neurons. Western blot analysis was performed to detect the expression of GABRA1 and NPTN both in vitro and in vivo. Immunofluorescence co-localization analysis and co-immunoprecipitation were performed to evaluate the interaction between GABRA1 and NPTN.
resultsThe expression of GABRA1 was found to be decreased on the neuronal surface both in vivo and in vitro seizure models. In the in vitro seizure model, α1-containing GABAaRs showed increased internalization. NPTN expression was found to be positively correlated with GABRA1 expression on the neuronal surface both in vivo and in vitro seizure models. In addition, NPTN overexpression alleviated seizures and NPTN was shown to bind to GABRA1 to form protein complexes that can be disrupted during seizures in both in vivo and in vitro models. Furthermore, NPTN was found to inhibit the internalization of α1-containing GABAaRs in the in vitro seizure model.
conclusionOur findings provide evidence that NPTN may exert antiepileptic effects by binding to GABRA1 to inhibit the internalization of α1-containing GABAaRs.
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