Lamotrigine inhibits TRESK regulated by G-protein coupled receptor agonists

Dawon Kang, Gyu Tae Kim, Eun Jin Kim, Jun Ho La, Jeong Soon Lee, Eun Shin Lee, Jae Yong Park, Seong Geun Hong, Jaehee Han

Research output: Contribution to journalArticlepeer-review

45 Scopus citations


Dorsal root ganglion (DRG) neurons express mRNAs for numerous two-pore domain K+ (K2P) channels and G-protein coupled receptors (GPCR). Recent studies have shown that TRESK is a major background K+ channel in DRG neurons. Here, we demonstrate the pharmacological properties of TRESK, including GPCR agonist-induced effects on DRG neurons. TRESK mRNA was highly expressed in DRG compared to brain and spinal cord. Similar to cloned TRESK, native TRESK was inhibited by acid and arachidonic acid (AA), but not zinc. Native TRESK was also activated by GPCR agonists such as acetylcholine, glutamate, and histamine. The glutamate-activated TRESK was blocked by lamotrigine in DRG neurons. In COS-7 cells transfected with mouse TRESK, 30 μM lamotrigine inhibited TRESK by ∼50%. Since TRESK is target of modulation by acid, AA, GPCR agonists, and lamotrigine, it is likely to play an active role in the regulation of excitability in DRG neurons.

Original languageEnglish (US)
Pages (from-to)609-615
Number of pages7
JournalBiochemical and Biophysical Research Communications
Issue number3
StatePublished - Mar 14 2008
Externally publishedYes


  • G-protein coupled receptor
  • Ganglia
  • Lamotrigine
  • Tandem-pore domain potassium channel

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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