Regulation of voltage-gated sodium channel expression, control of excitability and implications for seizure generation

Richard Baines, Wei-Hsiang Lin

Research output: Contribution to journalArticlepeer-review

21 Downloads (Pure)

Abstract

Voltage-gated Na (Nav) channels are key regulators of neuronal excitability. The mammalian genome encodes multiple Navs, but reported channel kinetics greatly exceeds gene number. Recent studies have identified a range of post-transcriptional modifications that, combined, are sufficient to generate diversity in channel kinetics and expression level. These mechanisms include RNA-editing, alternative splicing, translational regulation and protein modification. Pharmacological block of Nav is a proven clinical approach to treat human epilepsy, but is now generally accepted to be exhausted for the development of next-generation antiepileptics. The molecular components that mediate post-transcriptional modification may, therefore, provide alternate targets for drug design and recent large-scale screens in Drosophila validate this approach.
Original languageEnglish
JournalCurrent Opinion in Physiology
Early online date27 Dec 2017
DOIs
Publication statusPublished - 2018

Keywords

  • Drosophila
  • Pumilio
  • Sodium channel
  • Splicing
  • translation
  • Epilepsy

Fingerprint

Dive into the research topics of 'Regulation of voltage-gated sodium channel expression, control of excitability and implications for seizure generation'. Together they form a unique fingerprint.

Cite this