ArticleNeuron2017
Regulation of Thalamic and Cortical Network Synchrony by Scn8a.
Article in Neuron, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.
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Who cites it
79 citing papers in PubMed, 132 citations in OpenAlex.
- Midline thalamic neurons show early hypersynchrony during absence seizures in mouse models.iScience · 2026Article
- Interpretable Machine Learning Identifies an Emergent Absence Seizure Mechanism.bioRxiv : the preprint server for biology · 2026Article
- Maternal immune activation disrupts epigenomic and functional maturation of cortical excitatory neurons.Molecular psychiatry · 2026Article
- Transplantation of human iPSC-derived microglia ameliorates neuropathology and circuit dysfunction in progranulin-deficient mice.Molecular neurodegeneration · 2026Article
- Beyond seizure control: Identifying deficits in cognitive networks in absence epilepsy.Science advances · 2026Article
- Transplantation of Human IPSC-derived Microglia Ameliorates Neuropathology and Circuit Dysfunction in Progranulin-Deficient Mice.Research square · 2026Article
- Base editing rescues seizures and sudden death in a SCN8A mutation-associated developmental epileptic encephalopathy model.The Journal of clinical investigation · 2026Article
- The Thalamic Reticular Ultimatum: Carbamazepine's Betrayal in Absence Epileptic Seizures.Neuroscience bulletin · 2026Article
- Transplantation of Human IPSC-derived Microglia Ameliorates Neuropathology and Circuit Dysfunction in Progranulin-Deficient Mice.bioRxiv : the preprint server for biology · 2026Article
- A mouse model of GRIN2D developmental and epileptic encephalopathy recapitulates the human disease.Brain : a journal of neurology · 2026Article
- Absence seizures and sleep-wake abnormalities in a rat model of GRIN2B neurodevelopmental disorder.Epilepsia · 2025Article
- Synaptic dysregulation in a mouse model of GRIN2D developmental and epileptic encephalopathy.Brain : a journal of neurology · 2025Article
- Distilling Direct Effects via Conditional Differential Gene Expression Analysis.bioRxiv : the preprint server for biology · 2025Article
- Transgenic mouse models of sodium and potassium channelopathies in epilepsy: insights into disease mechanisms and therapeutics.Bioscience reports · 2025Review
- Local thalamic interneurons drive spindle termination and enable sleep-dependent learning.bioRxiv : the preprint server for biology · 2025Article
- Reticular thalamic hyperexcitability drives autism spectrum disorder behaviors in the Cntnap2 model of autism.Science advances · 2025Article
- A research roadmap for SCN8A-related disorders: addressing knowledge gaps and aligning research priorities across stakeholders.Orphanet journal of rare diseases · 2025Article
- Actions of the antiseizure drug carbamazepine in the thalamic reticular nucleus: Potential mechanism of aggravating absence seizures.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Non-parametric prediction of brain MRI microstructure using transfer learning.Imaging neuroscience (Cambridge, Mass.) · 2025Article
- Voltage-gated sodium channels in genetic epilepsy: up and down of excitability.Journal of neurochemistry · 2024Review
19 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Voltage-gated sodium channel (VGSC) mutations cause severe epilepsies marked by intermittent, pathological hypersynchronous brain states. Here we present two mechanisms that help to explain how mutations in one VGSC gene, Scn8a, contribute to two distinct seizure phenotypes: (1) hypoexcitation of cortical circuits leading to convulsive seizure resistance, and (2) hyperexcitation of thalamocortical circuits leading to non-convulsive absence epilepsy. We found that loss of Scn8a leads to altered RT cell intrinsic excitability and a failure in recurrent RT synaptic inhibition. We propose that these deficits cooperate to enhance thalamocortical network synchrony and generate pathological oscillations. To our knowledge, this finding is the first clear demonstration of a pathological state tied to disruption of the RT-RT synapse. Our observation that loss of a single gene in the thalamus of an adult wild-type animal is sufficient to cause spike-wave discharges is striking and represents an example of absence epilepsy of thalamic origin.
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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.