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 journalArticle

36 Citations (Scopus)

Abstract

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
Volume367
Issue number3
DOIs
StatePublished - Mar 14 2008
Externally publishedYes

Fingerprint

Spinal Ganglia
G-Protein-Coupled Receptors
Neurons
Arachidonic Acid
Glutamic Acid
Messenger RNA
Acids
COS Cells
Histamine
Acetylcholine
Zinc
Brain
Modulation
lamotrigine
Spinal Cord
Pharmacology

Keywords

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

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

Cite this

Lamotrigine inhibits TRESK regulated by G-protein coupled receptor agonists. / Kang, Dawon; Kim, Gyu Tae; Kim, Eun Jin; La, Jun-Ho; Lee, Jeong Soon; Lee, Eun Shin; Park, Jae Yong; Hong, Seong Geun; Han, Jaehee.

In: Biochemical and Biophysical Research Communications, Vol. 367, No. 3, 14.03.2008, p. 609-615.

Research output: Contribution to journalArticle

Kang, Dawon ; Kim, Gyu Tae ; Kim, Eun Jin ; La, Jun-Ho ; Lee, Jeong Soon ; Lee, Eun Shin ; Park, Jae Yong ; Hong, Seong Geun ; Han, Jaehee. / Lamotrigine inhibits TRESK regulated by G-protein coupled receptor agonists. In: Biochemical and Biophysical Research Communications. 2008 ; Vol. 367, No. 3. pp. 609-615.
@article{047b5563fc814760842e39e487e02f0d,
title = "Lamotrigine inhibits TRESK regulated by G-protein coupled receptor agonists",
abstract = "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.",
keywords = "G-protein coupled receptor, Ganglia, Lamotrigine, Tandem-pore domain potassium channel",
author = "Dawon Kang and Kim, {Gyu Tae} and Kim, {Eun Jin} and Jun-Ho La and Lee, {Jeong Soon} and Lee, {Eun Shin} and Park, {Jae Yong} and Hong, {Seong Geun} and Jaehee Han",
year = "2008",
month = "3",
day = "14",
doi = "10.1016/j.bbrc.2008.01.008",
language = "English (US)",
volume = "367",
pages = "609--615",
journal = "Biochemical and Biophysical Research Communications",
issn = "0006-291X",
publisher = "Academic Press Inc.",
number = "3",

}

TY - JOUR

T1 - Lamotrigine inhibits TRESK regulated by G-protein coupled receptor agonists

AU - Kang, Dawon

AU - Kim, Gyu Tae

AU - Kim, Eun Jin

AU - La, Jun-Ho

AU - Lee, Jeong Soon

AU - Lee, Eun Shin

AU - Park, Jae Yong

AU - Hong, Seong Geun

AU - Han, Jaehee

PY - 2008/3/14

Y1 - 2008/3/14

N2 - 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.

AB - 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.

KW - G-protein coupled receptor

KW - Ganglia

KW - Lamotrigine

KW - Tandem-pore domain potassium channel

UR - http://www.scopus.com/inward/record.url?scp=38749093319&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=38749093319&partnerID=8YFLogxK

U2 - 10.1016/j.bbrc.2008.01.008

DO - 10.1016/j.bbrc.2008.01.008

M3 - Article

VL - 367

SP - 609

EP - 615

JO - Biochemical and Biophysical Research Communications

JF - Biochemical and Biophysical Research Communications

SN - 0006-291X

IS - 3

ER -