ArticleProceedings of the National Academy of Sciences of the United States of America2022
Neuronal mechanism of a BK channelopathy in absence epilepsy and dyskinesia.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 30 citations in OpenAlex.
- Beyond seizure control: Identifying deficits in cognitive networks in absence epilepsy.Science advances · 2026Article
- Precision acupuncture for chemotherapy-induced peripheral neuropathy: multitarget mechanisms and integrated clinical translation framework.Frontiers in neurology · 2026Review
- Magnesium Ions as Modulators of Voltage-Gated and Ligand-Gated Ion Channels in Central Neurons.International journal of molecular sciences · 2025Review
- BK channel activity in skin fibroblasts from patients with neurological disorder.Channels (Austin, Tex.) · 2025Article
- Neuronal autophagy controls excitability via ryanodine receptor-mediated regulation of calcium-activated potassium channel function.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Calcium-activated ion channels drive atypical inhibition in medial habenula neurons.Science advances · 2025Article
- Article
- Evaluation of fourChannels (Austin, Tex.) · 2024Article
- Structural mapping of patient-associated KCNMA1 gene variants.Biophysical journal · 2024Article
- Attenuating midline thalamus bursting to mitigate absence epilepsy.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Large conductance voltage-and calcium-activated KFrontiers in pharmacology · 2024Review
- Disease-associated KCNMA1 variants decrease circadian clock robustness in channelopathy mouse models.The Journal of general physiology · 2023Article
- A neuron-specific Isca1 knockout rat developments multiple mitochondrial dysfunction syndromes.Animal models and experimental medicine · 2023Article
- CaInternational journal of molecular sciences · 2023Review
- Article
- BK Channel Gating Mechanisms: Progresses Toward a Better Understanding of Variants Linked Neurological Diseases.Frontiers in physiology · 2021Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A growing number of gain-of-function (GOF) BK channelopathies have been identified in patients with epilepsy and movement disorders. Nevertheless, the underlying pathophysiology and corresponding therapeutics remain obscure. Here, we utilized a knock-in mouse model carrying human BK-D434G channelopathy to investigate the neuronal mechanism of BK GOF in the pathogenesis of epilepsy and dyskinesia. The BK-D434G mice manifest the clinical features of absence epilepsy and exhibit severe motor deficits and dyskinesia-like behaviors. The cortical pyramidal neurons and cerebellar Purkinje cells from the BK-D434G mice show hyperexcitability, which likely contributes to the pathogenesis of absence seizures and paroxysmal dyskinesia. A BK channel blocker, paxilline, potently suppresses BK-D434G–induced hyperexcitability and effectively mitigates absence seizures and locomotor deficits in mice. Our study thus uncovered a neuronal mechanism of BK GOF in absence epilepsy and dyskinesia. Our findings also suggest that BK inhibition is a promising therapeutic strategy for mitigating BK GOF-induced neurological disorders.
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