ArticleProceedings of the National Academy of Sciences of the United States of America2014
Impaired excitability of somatostatin- and parvalbumin-expressing cortical interneurons in a mouse model of Dravet syndrome.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 154 papers.
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Who cites it
154 citing papers in PubMed, 287 citations in OpenAlex.
- The Role of Anterior Insular Parvalbumin GABAergic Interneurons in Impulsivity-Related and Alcohol-Seeking Behaviors.CNS neuroscience & therapeutics · 2026Article
- Convergent Inhibitory Cortical Circuit Disruption Drives Genetically Distinct Absence Seizures.bioRxiv : the preprint server for biology · 2026Article
- Exploring Linalool-Based Phytotherapy for Excitatory/Inhibitory Imbalance in Alzheimer's Disease: A Review of Lavender and Cannabis Therapeutic Effects on Sleep, Seizures, and Cognition.Phytotherapy research : PTR · 2026Review
- Axon Initial Segment: Structure, Biological Functions, Diseases, and Therapeutic Targets.MedComm · 2026Review
- Ameliorating Seizures in Dravet Syndrome: A Review of Newly Approved and Investigational Drugs, RNA and Gene-Based Therapies.CNS drugs · 2026Review
- Cortical Somatostatin Neurons Regulate Seizure Susceptibility via MINAR1/Gαs-cAMP Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Article
- SST interneuron maturation extends beyond the second postnatal week and is driven by coordinated transcriptional and functional remodeling.Frontiers in molecular neuroscience · 2026Article
- Medial septum parvalbumin-expressing inhibitory neurons are impaired in a mouse model of Dravet syndrome.Epilepsia · 2025Article
- Transgenic mouse models of sodium and potassium channelopathies in epilepsy: insights into disease mechanisms and therapeutics.Bioscience reports · 2025Review
- Cannabidiol dampens propagation of hippocampal hyperactivity and differentially modulates feedforward and feedback inhibition.bioRxiv : the preprint server for biology · 2025Article
- Deficiency of calretinin in prefrontal cortex causes behavioral deficits relevant to autism spectrum disorder in mice.Molecular brain · 2025Article
- Inhibition of the GSK3β/Nav1.6 complex suppresses early-stage Alzheimer's hyperexcitability.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Emerging Insights into the Pathogenic Mechanisms of Dravet Syndrome.Neurochemical research · 2025Review
- Spotlight on mechanism of sudden unexpected death in epilepsy in Dravet syndrome.Translational psychiatry · 2025Review
- Perirhinal cortex abnormalities impair hippocampal plasticity and learning inScience advances · 2025Article
- Ion channels and G protein-coupled receptors: Cannabidiol actions on disorders of excitability and synaptic excitatory-inhibitory ratio.Molecular pharmacology · 2025Review
- Synaptic Vesicle Glycoprotein 2A Knockout in Parvalbumin and Somatostatin Interneurons Drives Seizures in the Postnatal Mouse Brain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Parvalbumin interneurons: the dark and bright sides of a key playmaker of neural circuits and behavior.Frontiers in cellular neuroscience · 2025Review
- Activation of GLP-1R modulates the spontaneous discharge of nigral dopaminergic neurons and motor behavior in mice with chronic MPTP Parkinson's disease.Frontiers in aging neuroscience · 2025Article
94 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Haploinsufficiency of the voltage-gated sodium channel NaV1.1 causes Dravet syndrome, an intractable developmental epilepsy syndrome with seizure onset in the first year of life. Specific heterozygous deletion of NaV1.1 in forebrain GABAergic-inhibitory neurons is sufficient to cause all the manifestations of Dravet syndrome in mice, but the physiological roles of specific subtypes of GABAergic interneurons in the cerebral cortex in this disease are unknown. Voltage-clamp studies of dissociated interneurons from cerebral cortex did not detect a significant effect of the Dravet syndrome mutation on sodium currents in cell bodies. However, current-clamp recordings of intact interneurons in layer V of neocortical slices from mice with haploinsufficiency in the gene encoding the NaV1.1 sodium channel, Scn1a, revealed substantial reduction of excitability in fast-spiking, parvalbumin-expressing interneurons and somatostatin-expressing interneurons. The threshold and rheobase for action potential generation were increased, the frequency of action potentials within trains was decreased, and action-potential firing within trains failed more frequently. Furthermore, the deficit in excitability of somatostatin-expressing interneurons caused significant reduction in frequency-dependent disynaptic inhibition between neighboring layer V pyramidal neurons mediated by somatostatin-expressing Martinotti cells, which would lead to substantial disinhibition of the output of cortical circuits. In contrast to these deficits in interneurons, pyramidal cells showed no differences in excitability. These results reveal that the two major subtypes of interneurons in layer V of the neocortex, parvalbumin-expressing and somatostatin-expressing, both have impaired excitability, resulting in disinhibition of the cortical network. These major functional deficits are likely to contribute synergistically to the pathophysiology of Dravet syndrome.
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Registered trials
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