Interactions between GABA-B1 receptors and Kir 3 inwardly rectifying potassium channels

Martin David; Maxime Richer; Aida M. Mamarbachi; Louis R. Villeneuve; Denis J. Dupré; Terence E. Hebert

doi:10.1016/j.cellsig.2006.05.014

Interactions between GABA-B₁ receptors and Kir 3 inwardly rectifying potassium channels

Martin David, Maxime Richer, Aida M. Mamarbachi, Louis R. Villeneuve, Denis J. Dupré, Terence E. Hebert

Research output: Contribution to journal › Article › peer-review

59 Citations (Scopus)

Abstract

γ-aminobutyric acid (GABA) is the principal inhibitory neurotransmitter in the mammalian brain. It acts via both ionotropic GABA-A and metabotropic GABA-B receptors. We evaluated the interaction of receptors with members of the inwardly rectifying potassium (Kir 3) channel family, which also play an important role in neuronal transmission and membrane excitability. These channels are functionally regulated by GABA-B receptors. Possible physical interactions between GABA-B receptor and Kir 3 channels expressed in HEK cells were evaluated using Bioluminescence Resonance Energy Transfer (BRET) experiments, co-immunoprecipitation and confocal microscopy. Our data indicate that Kir 3 channels and Gβγ subunits can interact with the GABA-B₁ subunits independently of the GABA-B₂ subunit or Kir 3.4 which are ultimately responsible for their targetting to the cell surface. Thus signalling complexes containing GABA-B receptors, G proteins and Kir channels are formed shortly after biosynthesis most likely in the endoplasmic reticulum.

Original language	English
Pages (from-to)	2172-2181
Number of pages	10
Journal	Cellular Signalling
Volume	18
Issue number	12
DOIs	https://doi.org/10.1016/j.cellsig.2006.05.014
Publication status	Published - Dec 2006
Externally published	Yes

Bibliographical note

Funding Information:
This work was supported by grants from the Canadian Institutes of Health Research and Heart and Stroke Foundation of Quebec to T.E.H. T.E.H. holds a senior scholarship from the Fonds de Recherche en Santé du Québec. Flag-RaB 1 N124I was from Dr. Guangyu Wu (Louisiana State University Health Sciences Center, New Orleans, LA). The vsvg-Sar1 WT and vsvg-Sar1 T39N were from Dr. Phil Wedegaertner (Thomas Jefferson University, Philadelphia, PA); GFP-Gγ 2 was obtained from Dr. Céline Galès and Dr. Michel Bouvier (Université de Montréal, Montréal, Canada). We thank Victor Rebois and Céline Galès for helpful discussion.

ASJC Scopus Subject Areas

Cell Biology

PubMed: MeSH publication types

Journal Article
Research Support, Non-U.S. Gov't

Access to Document

10.1016/j.cellsig.2006.05.014

Cite this

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title = "Interactions between GABA-B1 receptors and Kir 3 inwardly rectifying potassium channels",

abstract = "γ-aminobutyric acid (GABA) is the principal inhibitory neurotransmitter in the mammalian brain. It acts via both ionotropic GABA-A and metabotropic GABA-B receptors. We evaluated the interaction of receptors with members of the inwardly rectifying potassium (Kir 3) channel family, which also play an important role in neuronal transmission and membrane excitability. These channels are functionally regulated by GABA-B receptors. Possible physical interactions between GABA-B receptor and Kir 3 channels expressed in HEK cells were evaluated using Bioluminescence Resonance Energy Transfer (BRET) experiments, co-immunoprecipitation and confocal microscopy. Our data indicate that Kir 3 channels and Gβγ subunits can interact with the GABA-B1 subunits independently of the GABA-B2 subunit or Kir 3.4 which are ultimately responsible for their targetting to the cell surface. Thus signalling complexes containing GABA-B receptors, G proteins and Kir channels are formed shortly after biosynthesis most likely in the endoplasmic reticulum.",

author = "Martin David and Maxime Richer and Mamarbachi, {Aida M.} and Villeneuve, {Louis R.} and Dupr{\'e}, {Denis J.} and Hebert, {Terence E.}",

note = "Funding Information: This work was supported by grants from the Canadian Institutes of Health Research and Heart and Stroke Foundation of Quebec to T.E.H. T.E.H. holds a senior scholarship from the Fonds de Recherche en Sant{\'e} du Qu{\'e}bec. Flag-RaB 1 N124I was from Dr. Guangyu Wu (Louisiana State University Health Sciences Center, New Orleans, LA). The vsvg-Sar1 WT and vsvg-Sar1 T39N were from Dr. Phil Wedegaertner (Thomas Jefferson University, Philadelphia, PA); GFP-Gγ 2 was obtained from Dr. C{\'e}line Gal{\`e}s and Dr. Michel Bouvier (Universit{\'e} de Montr{\'e}al, Montr{\'e}al, Canada). We thank Victor Rebois and C{\'e}line Gal{\`e}s for helpful discussion.",

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AU - Dupré, Denis J.

AU - Hebert, Terence E.

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N2 - γ-aminobutyric acid (GABA) is the principal inhibitory neurotransmitter in the mammalian brain. It acts via both ionotropic GABA-A and metabotropic GABA-B receptors. We evaluated the interaction of receptors with members of the inwardly rectifying potassium (Kir 3) channel family, which also play an important role in neuronal transmission and membrane excitability. These channels are functionally regulated by GABA-B receptors. Possible physical interactions between GABA-B receptor and Kir 3 channels expressed in HEK cells were evaluated using Bioluminescence Resonance Energy Transfer (BRET) experiments, co-immunoprecipitation and confocal microscopy. Our data indicate that Kir 3 channels and Gβγ subunits can interact with the GABA-B1 subunits independently of the GABA-B2 subunit or Kir 3.4 which are ultimately responsible for their targetting to the cell surface. Thus signalling complexes containing GABA-B receptors, G proteins and Kir channels are formed shortly after biosynthesis most likely in the endoplasmic reticulum.

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