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Related Experiment Video

Updated: May 14, 2026

Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents

Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca²⁺ Transients and Membrane Currents

Published on: July 3, 2013

'Eventless' InsP3-dependent SR-Ca2+ release affecting atrial Ca2+ sparks.

Tamara Horn¹, Nina D Ullrich, Marcel Egger

¹Department of Physiology, University of Bern, Bühlplatz 5, CH-3012 Bern, Switzerland.

The Journal of Physiology

|February 6, 2013

Summary

Augmented inositol 1,4,5-trisphosphate receptor (InsP3R) function impacts cardiac arrhythmia. This study reveals that InsP3R-induced Ca2+ release modulates ryanodine receptor (RyR) function and Ca2+ sparks in atrial myocytes.

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Evaluation of Synaptic Multiplicity Using Whole-cell Patch-clamp Electrophysiology

Evaluation of Synaptic Multiplicity Using Whole-cell Patch-clamp Electrophysiology

Published on: April 23, 2019

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Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents

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Published on: July 3, 2013

Evaluation of Synaptic Multiplicity Using Whole-cell Patch-clamp Electrophysiology

Evaluation of Synaptic Multiplicity Using Whole-cell Patch-clamp Electrophysiology

Published on: April 23, 2019

Area of Science:

Cardiovascular Physiology
Cellular Biology
Molecular Cardiology

Background:

Augmented inositol 1,4,5-trisphosphate receptor (InsP3R) function is implicated in cardiac pathologies like arrhythmia.
The role of InsP3R-induced Ca2+ release (IP3ICR) in excitation-contraction coupling (ECC) is debated under physiological and pathological conditions.

Purpose of the Study:

To investigate the hypothesis that local IP3ICR directly influences ryanodine receptor (RyR) function and subsequent Ca2+ release in atrial myocytes.
To elucidate the cross-talk mechanism between InsP3Rs and RyRs in cardiac cells.

Main Methods:

Whole-cell voltage-clamp technique in isolated atrial myocytes from C57/BL6 mice.
UV-flash photolysis of caged InsP3 to evoke IP3ICR.
Ca2+ spark analysis and pharmacological agents (2-aminoethoxydiphenyl borate, xestospongin C, tetracaine) to differentiate RyR and InsP3R activity.
Sarcoplasmic reticulum (SR) Ca2+ leak/load measurements.

Main Results:

Photolytic InsP3 release significantly increased Ca2+ release event frequency, identified as Ca2+ sparks originating from RyR openings.
Pharmacological separation confirmed the involvement of both RyRs and InsP3Rs in SR Ca2+ release.
InsP3R-mediated SR Ca2+ flux was characterized as eventless, contrasting with RyR-dependent Ca2+ sparks.
IP3ICR was shown to effectively modulate RyR openings and Ca2+ spark probability.

Conclusions:

Eventless and efficient InsP3-dependent SR Ca2+ flux is a primary mechanism for functional cross-talk between InsP3Rs and RyRs.
This cross-talk mechanism may significantly influence ECC sensitivity in atrial myocytes.
Understanding this interaction is crucial for addressing cardiac pathologies linked to InsP3R dysfunction.