In vivo expression of G-protein beta1gamma2 dimer in adult mouse skeletal muscle alters L-type calcium current and excitation-contraction coupling.

Norbert Weiss, Claude Legrand, Sandrine Pouvreau, Hicham Bichraoui, Bruno Allard, Gerald W. Zamponi, Michel De Waard, Vincent Jacquemond
The Journal of Physiology. 2010-08-01; 588(15): 2945-2960
DOI: 10.1113/jphysiol.2010.191593

PubMed
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A number of G‐protein‐coupled receptors are expressed in skeletal muscle but their roles in muscle physiology and downstream effector systems remain poorly investigated. Here we explored the functional importance of the G‐protein βγ (Gβγ) signalling pathway on voltage‐controlled Ca2+ homeostasis in single isolated adult skeletal muscle fibres. A GFP‐tagged Gβ1γ2 dimer was expressed in vivo in mice muscle fibres. The GFP fluorescence pattern was consistent with a Gβ1γ2 dimer localization in the transverse‐tubule membrane. Membrane current and indo‐1 fluorescence measurements performed under voltage‐clamp conditions reveal a drastic reduction of both L‐type Ca2+ current density and of peak amplitude of the voltage‐activated Ca2+ transient in Gβ1γ2‐expressing fibres. These effects were not observed upon expression of Gβ2γ2, Gβ3γ2 or Gβ4γ2. Our data suggest that the G‐protein β1γ2 dimer may play an important regulatory role in skeletal muscle excitation–contraction coupling.

Auteurs Bordeaux Neurocampus