Quinidine normalizes the open duration of slow-channel mutants of the acetylcholine receptor

Takayasu Fukudome, Kinji Ohno, Joan M. Brengman, Andrew G. Engel

Research output: Contribution to journalArticlepeer-review

47 Scopus citations

Abstract

QUINIDINE is a long-lived open-channel blocker of the wild-type endplate acetylcholine receptor (AChR). To test the hypothesis that quinidine can normalize the prolonged channel opening events of slow-channel mutants of human AChR, we expressed wild-type AChR and five well characterized slow- channel mutants of AChR in HEK 293 cells and monitored the effects of quinidine on acetylcholine-induced channel currents. Quinidine shortens the longest component of channel opening burst (τ(3b)) of both wild-type and mutant AChRs in a concentration-dependent manner, and 5 μM quinidine reduces τ(3b) of the mutant AChRs to that of wild-type AChRs in the absence of quinidine. Because this concentration of quinidine is attainable in clinical practice, the findings predict a therapeutic effect for quinidine in the slow-channel congenital myasthenic syndrome.

Original languageEnglish (US)
Pages (from-to)1907-1911
Number of pages5
JournalNeuroReport
Volume9
Issue number8
DOIs
StatePublished - Jun 1 1998

Keywords

  • Acetylcholine receptor
  • Channel block
  • Patch-clamp
  • Quinidine
  • Slow channel congenital myasthenic syndrome

ASJC Scopus subject areas

  • Neuroscience(all)

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