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Updated: Jul 18, 2026

Methods for the Isolation, Culture, and Functional Characterization of Sinoatrial Node Myocytes from Adult Mice
Published on: October 23, 2016
TRPM4, a Ca2+-activated nonselective cation channel in mouse sino-atrial node cells
Marie Demion1, Patrick Bois, Pierre Launay
1Institut de Physiologie et Biologie Cellulaires, CNRS UMR 6187, Université de Poitiers, F-86022 Poitiers Cedex, France.
Calcium-activated nonselective cation channels (NSC(Ca)), identified as TRPM4, are present in mouse sino-atrial node cells. This discovery suggests TRPM4 channels play a role in regulating heart rhythm.
Area of Science:
- Cardiology
- Molecular Biology
- Electrophysiology
Background:
- Calcium-activated nonselective cation channels (NSC(Ca)) are implicated in cardiac electrophysiological perturbations, particularly in ventricular hypertrophy.
- While the pacemaker I(f) current is a known factor, the role of NSC(Ca) in heart rhythm regulation, including in specialized sino-atrial node (SAN) cells, requires investigation.
Purpose of the Study:
- To detect and characterize NSC(Ca) activity in mouse SAN cells.
- To determine if the TRPM4 channel, a member of the TRP melastatin subfamily, is expressed and functional in SAN cells.
Main Methods:
- Patch-clamp technique (inside-out configuration) on freshly isolated adult mouse SAN cells.
- Reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting to confirm TRPM4 mRNA and protein expression.
Main Results:
- NSC(Ca) activity was detected in mouse SAN cells, exhibiting voltage dependence and a conductance of 20.9±0.5 pS.
- The channel is permeable to Na+ and K+ but not Ca2+, activated by intracellular calcium, and inhibited by intracellular ATP and glibenclamide.
- TRPM4 mRNA and protein were confirmed in SAN cells, and the channel showed sensitivity to phosphatidylinositol 4,5-bisphosphate, flufenamic acid, and glibenclamide.
Conclusions:
- TRPM4 channels are functionally expressed in mouse SAN cells.
- TRPM4 channels may be crucial in the generation and modulation of cardiac rhythm.
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