Na+ channelopathies and epilepsy: recent advances and new perspectives

No abstract is available for this paper.

• Publication year

  2010

• Venue

  Expert Review of Clinical Pharmacology

• Publication date

  2010-05-01

• Fields of study

  Medicine

• Identifiers
  DOI 10.1586/ecp.10.20PMID 22111617
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• Altered Function of the SCN1A Voltage-gated Sodium Channel Leads to γ-Aminobutyric Acid-ergic (GABAergic) Interneuron Abnormalities*

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• Novel treatments in epilepsy guided by genetic diagnosis

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• The Effects of Hydro-Alcoholic Extracts of Glycyrrhiza inflata for Review on Voltage-Gated Sodium Channel Subtype 1.4

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• Gain of Function for the SCN1A/hNav1.1-L1670W Mutation Responsible for Familial Hemiplegic Migraine

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• Features of the broader autism phenotype in people with epilepsy support shared mechanisms between epilepsy and autism spectrum disorder

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• Evaluation of Presumably Disease Causing SCN1A Variants in a Cohort of Common Epilepsy Syndromes

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• What are the arguments for and against rational therapy for epilepsy?

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• Impaired Action Potential Initiation in GABAergic Interneurons Causes Hyperexcitable Networks in an Epileptic Mouse Model Carrying a Human NaV1.1 Mutation

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• Epileptogenic ion channel mutations: from bedside to bench and, hopefully, back again.

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