ArticleEpilepsia open2020
Persistent sodium current blockers can suppress seizures caused by loss of low-threshold D-type potassium currents: Predictions from an in silico study of K
Article in Epilepsia open, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 10 citations in OpenAlex.
- Roles of KCNA2 in Neurological Diseases: from Physiology to Pathology.Molecular neurobiology · 2024Review
- Unusual Voltage-Gated Sodium and Potassium Channelopathies Related to Epilepsy.Journal of clinical neurology (Seoul, Korea) · 2024Article
- The Role of Glutamate Receptors in Epilepsy.Biomedicines · 2023Review
- Ranolazine Interacts Antagonistically with Some Classical Antiepileptic Drugs-An Isobolographic Analysis.Molecules (Basel, Switzerland) · 2022Article
- The Potential Role of Polyamines in Epilepsy and Epilepsy-Related Pathophysiological Changes.Biomolecules · 2022Review
- Article
- Clinical and Functional Study of a De Novo Variant in the PVP Motif of Kv1.1 Channel Associated with Epilepsy, Developmental Delay and Ataxia.International journal of molecular sciences · 2022Article
- Therapeutic Potential of Sodium Channel Blockers as a Targeted Therapy Approach inFrontiers in neurology · 2021Article
- Kv1.1 Channelopathies: Pathophysiological Mechanisms and Therapeutic Approaches.International journal of molecular sciences · 2020Review
- Persistent sodium current blockers can suppress seizures caused by loss of low-threshold D-type potassium currents: Predictions from an in silico study of KEpilepsia open · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveIon channels belonging to subfamily A of voltage-gated potassium channels (K
methodsWe used a novel in silico model, the laminar cortex model (LCM), to examine changes in neuronal excitability and network dynamics associated with loss-of-function mutations in K
resultsReduced axonal D-type currents led to lower firing threshold and widened action potentials, both lowering the seizure threshold. Two potential therapeutic targets for treating seizures caused by loss-of-function changes in K SIGNIFICANCE: Riluzole reduces persistent sodium currents and excitatory postsynaptic currents from NMDA receptor activation. Our results suggest that this FDA-approved drug can be repurposed to treat epilepsies caused by mutations affecting axonal K
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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.