ArticleSleep2020
Electrophysiological features of sleep in children with Kir4.1 channel mutations and Autism-Epilepsy phenotype: a preliminary study.
Article in Sleep, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.
- Bridging Genetic Insights with Neuroimaging in Autism Spectrum Disorder-A Systematic Review.International journal of molecular sciences · 2024Pooled it
- Aberrant astroglial Kir4.1 activation in the anterior cingulate cortex disrupts neuronal excitability and social behavior.Acta pharmaceutica Sinica. B · 2026Article
- Astroglial Kir4.1 and AQP4 Channels: Key Regulators of Potassium Homeostasis and Their Implications in Autism Spectrum Disorders.Cellular and molecular neurobiology · 2025Review
- Emotional Dysregulation and Sleep Problems: A Transdiagnostic Approach in Youth.Clinics and practice · 2024Article
- Review
- From Physiology to Pathology of Cortico-Thalamo-Cortical Oscillations: Astroglia as a Target for Further Research.Frontiers in neurology · 2021Review
- Local Sleep and Alzheimer's Disease Pathophysiology.Frontiers in neuroscience · 2020Review
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
STUDY
objectivesRecently, a role for gain-of-function (GoF) mutations of the astrocytic potassium channel Kir4.1 (KCNJ10 gene) has been proposed in subjects with Autism-Epilepsy phenotype (AEP). Epilepsy and autism spectrum disorder (ASD) are common and complexly related to sleep disorders. We tested whether well characterized mutations in KCNJ10 could result in specific sleep electrophysiological features, paving the way to the discovery of a potentially relevant biomarker for Kir4.1-related disorders.
methodsFor this case-control study, we recruited seven children with ASD either comorbid or not with epilepsy and/or EEG paroxysmal abnormalities (AEP) carrying GoF mutations of KCNJ10 and seven children with similar phenotypes but wild-type for the same gene, comparing period-amplitude features of slow waves detected by fronto-central bipolar EEG derivations (F3-C3, F4-C4, and Fz-Cz) during daytime naps.
resultsChildren with Kir4.1 mutations displayed longer slow waves periods than controls, in Fz-Cz (mean period = 112,617 ms ± SE = 0.465 in mutated versus mean period = 105,249 ms ± SE = 0.375 in controls, p < 0.001). An analog result was found in F3-C3 (mean period = 125,706 ms ± SE = 0.397 in mutated versus mean period = 120,872 ms ± SE = 0.472 in controls, p < 0.001) and F4-C4 (mean period = 127,914 ms ± SE = 0.557 in mutated versus mean period = 118,174 ms ± SE = 0.442 in controls, p < 0.001).
conclusionThis preliminary finding suggests that period-amplitude slow wave features are modified in subjects carrying Kir4.1 GoF mutations. Potential clinical applications of this finding are discussed.
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