ArticleBiological psychiatry2017
Opposing Effects on Na
Article in Biological psychiatry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 164 papers, 2 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
164 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- A systematic review of non-coding RNA genes with differential expression profiles associated with autism spectrum disorders.PloS one · 2023Pooled it
- Genetic polymorphisms in SCN2A are not associated with epilepsy risk and AEDs response: evidence from a meta-analysis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2021Pooled it
- Functional and pharmacological characterization of theEpilepsy & behavior reports · 2026Article
- Nonsense-mediated decay influences position-dependent effects of SCN2A premature stop codons on neuronal excitability and behavior.Molecular psychiatry · 2026Article
- Altered oligodendroglial cell development and increased myelination in SCN2A gain-of-function-linked epilepsy.Acta neuropathologica communications · 2026Article
- Autism-associated SCN2A deficiency disrupts cortico-striatal circuitry in human brain assembloids.Neuron · 2026Article
- Lvguidingan inhibits Nav1.2 and epilepsy-associated SCN2A gain-of-function variants.Acta pharmacologica Sinica · 2026Article
- Review
- USP15 mutation associated with autism spectrum disorder alters progenitor fate and neuronal maturation in human brain organoids.Molecules and cells · 2026Article
- Voltage-Gated Sodium Channel NaBiochemical genetics · 2026Article
- Mapping lncRNAs onto multilevel mRNA co‑expression modules in autism.Translational psychiatry · 2026Article
- Voltage-gated sodium channels in the nervous system: Molecular physiology to therapeutic interventions.Neural regeneration research · 2026Article
- Excitatory Dysfunction and Phenotypic Rescue in a Human Neuronal Model ofbioRxiv : the preprint server for biology · 2026Article
- Mechanisms of SCN2A loss of function do not predict presence or phenotype of epilepsy.Epilepsia · 2026Article
- Linking rare variants to cell-type function in profound autism with brain transcriptomics and foundation models.Cell genomics · 2026Review
- Functional Characterization of a De NovoNeurology. Genetics · 2026Article
- Antisense oligonucleotides to KIF1A polymorphisms expand targets and rescue patient-derived neurons in vitro.Nature communications · 2026Article
- Neurologist's Black Swan: Molecular Basis of Prenatal Seizures.International journal of molecular sciences · 2025Review
- Degraded sensory coding in a mouse model ofbioRxiv : the preprint server for biology · 2025Article
- Review
104 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
backgroundVariants in the SCN2A gene that disrupt the encoded neuronal sodium channel Na
methodsWe examined the properties of 11 ASD-associated SCN2A variants in heterologous expression systems using whole-cell voltage-clamp electrophysiology and immunohistochemistry. Resultant data were incorporated into computational models of developing and mature cortical pyramidal cells that express Na
resultsIn contrast to gain of function variants that contribute to seizure, we found that all ASD-associated variants dampened or eliminated channel function. Incorporating these electrophysiological results into a compartmental model of developing excitatory neurons demonstrated that all ASD variants, regardless of their mechanism of action, resulted in deficits in neuronal excitability. Corresponding analysis of mature neurons predicted minimal change in neuronal excitability.
conclusionsThis functional characterization thus identifies SCN2A mutation and Na
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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.