ArticleProceedings of the National Academy of Sciences of the United States of America2012
Na(V)1.1 channels are critical for intercellular communication in the suprachiasmatic nucleus and for normal circadian rhythms.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
70 citing papers in PubMed, 1 synthesis or guideline pooled it, 100 citations in OpenAlex.
- Clock gene dysregulation in epilepsy: A systematic review.Epilepsia open · 2026Pooled it
- Hyperactivation of distinct thalamic nuclei differentially impairs sleep physiology in rats.Molecular psychiatry · 2026Article
- Lost in Sleep Transition: Tangled Sleep and Thermoregulation in Dravet Syndrome.Epilepsy currents · 2026Article
- Voltage-gated sodium channels in the nervous system: Molecular physiology to therapeutic interventions.Neural regeneration research · 2026Article
- Disrupted temperature-sleep coupling mechanism in a Dravet syndrome mouse model.Nature communications · 2026Article
- Circadian rhythms in pediatric neurocritical care: interfaces and opportunities.Frontiers in neurology · 2026Review
- Dim light at night disrupts the sleep-wake cycle and exacerbates abnormal EEG activity in Cntnap2 knockout mice: implications for autism spectrum disorders.Molecular autism · 2025Article
- Molecular Characterization of Hypothalamic-Pituitary-Ovarian Axis Regulation in the Manchurian Zokor (Genes · 2025Article
- Sleep Identification Enabled by Supervised Training Algorithms (SIESTA): An Open-Source Platform for Automatic Sleep Staging of Rodent Electrocorticographic and Electromyographic Data.Journal of biological rhythms · 2025Article
- Sudden Unexpected Death in Epilepsy: A Narrative Review of Mechanism, Risks, and Prevention.Journal of clinical medicine · 2025Review
- Spotlight on mechanism of sudden unexpected death in epilepsy in Dravet syndrome.Translational psychiatry · 2025Review
- The circadian molecular clock in the suprachiasmatic nucleus is necessary but not sufficient for fear entrainment.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Expression of the vesicular GABA transporter within neuromedin SProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Deficiency of autism-related Scn2a gene in mice disrupts sleep patterns and circadian rhythms.Neurobiology of disease · 2022Article
- Sudden unexpected death in epilepsy: Respiratory mechanisms.Handbook of clinical neurology · 2022Review
- Gpr19 is a circadian clock-controlled orphan GPCR with a role in modulating free-running period and light resetting capacity of the circadian clock.Scientific reports · 2021Article
- Clinical spectrum and the comorbidities of Dravet syndrome in Taiwan and the possible molecular mechanisms.Scientific reports · 2021Article
- Sodium channelopathies of skeletal muscle and brain.Physiological reviews · 2021Review
- Transfer ofMolecular therapy. Nucleic acids · 2021Article
- The role of GABAergic signalling in neurodevelopmental disorders.Nature reviews. Neuroscience · 2021Review
10 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
8 authors at 4 institutions in 3 countries.
Funding
Abstract
Na(V)1.1 is the primary voltage-gated Na(+) channel in several classes of GABAergic interneurons, and its reduced activity leads to reduced excitability and decreased GABAergic tone. Here, we show that Na(V)1.1 channels are expressed in the suprachiasmatic nucleus (SCN) of the hypothalamus. Mice carrying a heterozygous loss of function mutation in the Scn1a gene (Scn1a(+/-)), which encodes the pore-forming α-subunit of the Na(V)1.1 channel, have longer circadian period than WT mice and lack light-induced phase shifts. In contrast, Scn1a(+/-) mice have exaggerated light-induced negative-masking behavior and normal electroretinogram, suggesting an intact retina light response. Scn1a(+/-) mice show normal light induction of c-Fos and mPer1 mRNA in ventral SCN but impaired gene expression responses in dorsal SCN. Electrical stimulation of the optic chiasm elicits reduced calcium transients and impaired ventro-dorsal communication in SCN neurons from Scn1a(+/-) mice, and this communication is barely detectable in the homozygous gene KO (Scn1a(-/-)). Enhancement of GABAergic transmission with tiagabine plus clonazepam partially rescues the effects of deletion of Na(V)1.1 on circadian period and phase shifting. Our report demonstrates that a specific voltage-gated Na(+) channel and its associated impairment of SCN interneuronal communication lead to major deficits in the function of the master circadian pacemaker. Heterozygous loss of Na(V)1.1 channels is the underlying cause for severe myoclonic epilepsy of infancy; the circadian deficits that we report may contribute to sleep disorders in severe myoclonic epilepsy of infancy patients.
Indexed as
Identifiers
What OpenQuestion holds
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.