Related Experiment Video
Updated: Aug 7, 2026

In Vivo Calcium Imaging in C. elegans Body Wall Muscles
Published on: October 20, 2019
Sarcoplasmic reticulum Ca2+ release and depletion fail to affect sarcolemmal ion channel activity in mouse skeletal
Bruno Allard1, Harold Couchoux, Sandrine Pouvreau
1Physiologie Intégrative, Cellulaire et Moléculaire, UMR CNRS 5123, Université C. Bernard Lyon I, 43 bd du 11 Novembre 1918, 69622 Villeurbanne cedex, France.
Abstract:
In skeletal muscle, sarcoplasmic reticulum (SR) Ca2+ depletion is suspected to trigger a calcium entry across the plasma membrane and recent studies also suggest that the opening of channels spontaneously active at rest and possibly involved in Duchenne dystrophy may be regulated by SR Ca2+ depletion. Here we simultaneously used the cell-attached and whole-cell voltage-clamp techniques as well as intracellular Ca2+ measurements on single isolated mouse skeletal muscle fibres to unravel any possible change in membrane conductance that would depend upon SR Ca2+ release and/or SR Ca2+ depletion. Delayed rectifier K+ single channel activity was routinely detected during whole-cell depolarizing pulses. In addition the activity of channels carrying unitary inward currents of approximately 1.5 pA at -80 mV was detected in 17 out of 127 and in 21 out of 59 patches in control and mdx dystrophic fibres, respectively. In both populations of fibres, large whole-cell depolarizing pulses did not reproducibly increase this channel activity. This was also true when, repeated application of the whole-cell pulses led to exhaustion of the Ca2+ transient. SR Ca2+ depletion produced by the SR Ca2+ pump inhibitor cyclopiazonic acid (CPA) also failed to induce any increase in the resting whole-cell conductance and in the inward single channel activity. Overall results indicate that voltage-activated SR Ca2+ release and/or SR Ca2+ depletion are not sufficient to activate the opening of channels carrying inward currents at negative voltages and challenge the physiological relevance of a store-operated membrane conductance in adult skeletal muscle.
Related Concept Videos
Relaxation of Skeletal Muscles
When an action potential reaches the axon terminal, it depolarizes the membrane and opens voltage-gated sodium channels. Sodium ions enter the cell, further depolarizing the presynaptic membrane. This depolarization causes voltage-gated calcium channels to open.
Cross-bridge Cycle
Generation of Action Potential in Skeletal Muscles
Like neurons, muscle cells are also regarded as excitable due to their capacity to change in response to stimuli, primarily due to voltage-gated ion channels embedded in their plasma membranes, which get activated by alterations in the cell's...
Overview of Skeletal Muscle
Microscopic Anatomy of Skeletal Muscles
The muscle sarcolemma is a plasma membrane enclosing each muscle cell that conducts electrical signals called action potentials. The sarcolemma extends into the cell to form T-tubules, ensuring the neural impulses are uniformly distributed across the entire muscle...
Smooth Muscle Contraction
The onset of contraction is triggered by an increase in calcium ions within the sarcoplasm, similar to the process in striated muscle. However, smooth muscles have a relatively smaller reservoir of the sarcoplasmic...

