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

doi:10.1016/j.bbrc.2008.01.008

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 journal › Article › peer-review

46 Scopus citations

Abstract

Dorsal root ganglion (DRG) neurons express mRNAs for numerous two-pore domain K⁺ (K_2P) 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 language	English (US)
Pages (from-to)	609-615
Number of pages	7
Journal	Biochemical and Biophysical Research Communications
Volume	367
Issue number	3
DOIs	https://doi.org/10.1016/j.bbrc.2008.01.008
State	Published - Mar 14 2008
Externally published	Yes

Keywords

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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10.1016/j.bbrc.2008.01.008

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@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 La, {Jun Ho} and Lee, {Jeong Soon} and Lee, {Eun Shin} and Park, {Jae Yong} and Hong, {Seong Geun} and Jaehee Han",

note = "Funding Information: This work was supported by the Korea Research Foundation Grant funded by the Korean Government (KRF-2006-11-E00158, KRF-2006-005-J04204), and partially supported by the Basic Research Program of the KOSEF (R13-2005-012-01002-0). Copyright: Copyright 2009 Elsevier B.V., All rights reserved.",

year = "2008",

month = mar,

day = "14",

doi = "10.1016/j.bbrc.2008.01.008",

language = "English (US)",

volume = "367",

pages = "609--615",

journal = "Biochemical and Biophysical Research Communications",

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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

N1 - Funding Information: This work was supported by the Korea Research Foundation Grant funded by the Korean Government (KRF-2006-11-E00158, KRF-2006-005-J04204), and partially supported by the Basic Research Program of the KOSEF (R13-2005-012-01002-0). Copyright: Copyright 2009 Elsevier B.V., All rights reserved.

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

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JO - Biochemical and Biophysical Research Communications

JF - Biochemical and Biophysical Research Communications

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ER -

Lamotrigine inhibits TRESK regulated by G-protein coupled receptor agonists

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