author={Angela F. Dulhunty},
  journal={Clinical and Experimental Pharmacology and Physiology},
  • A. Dulhunty
  • Published 1 September 2006
  • Biology
  • Clinical and Experimental Pharmacology and Physiology
1 Excitation–contraction coupling is broadly defined as the process linking the action potential to contraction in striated muscle or, more narrowly, as the process coupling surface membrane depolarization to Ca2+ release from the sarcoplasmic reticulum. 2 We now know that excitation–contraction coupling depends on a macromolecular protein complex or ‘calcium release unit’. The complex extends the extracellular space within the transverse tubule invaginations of the surface membrane, across the… 
Voltage sensing mechanism in skeletal muscle excitation-contraction coupling: coming of age or midlife crisis?
Early and recent findings are presented that support and define the role of Cav1.1 as a voltage sensor for ECC, two essential players of ECC in skeletal muscle.
Spatio-temporal calcium dynamics in pacemaking units of the interstitial cells of Cajal.
In vitro exploration of interactions between junctin and the Ryanodine receptor from skeletal and cardiac muscle
The study demonstrates that junctin regulates RyRI and RyR2 via interactions in both the cytoplasm and SR lumen, the combined actions of Njun and Cjun indicate that the RyR inhibition induced by luminal addition of Cjun was not altered by subsequent addition ofNjun to the cy toplasmic solution.
Calcium influx through a possible coupling of cation channels impacts skeletal muscle satellite cell activation in response to mechanical stretch.
Evidence is added that two ion channels, the mechanosensitive cation channel (MS channel) and the long-lasting-type voltage-gated calcium-ion channel (L-V GC channel), mediate the influx of extracellular calcium ions in response to cyclic stretch in satellite cell cultures, providing an additional insight that calcium ions may flow in through L-VGC channels by possible coupling with adjacent MS channel gating that promotes the local depolarization of cell membranes.
Mechanisms of excitation-contraction uncoupling relevant to activity-induced muscle fatigue.
  • G. Lamb
  • Biology
    Applied physiology, nutrition, and metabolism = Physiologie appliquee, nutrition et metabolisme
  • 2009
It appears that the disruption to the coupling occurs at the triad junction, where the voltage-sensor molecules (dihydropyridine receptors) normally interact with and open the Ca2+ release channels (ryanodine receptors) in the adjacent sarcoplasmic reticulum (SR).
Local calcium signals induced by hyper-osmotic stress in mammalian skeletal muscle cells
The results point to a modulatory, even though not essential, role of the DHP receptor for osmotic stress-induced Ca signals in skeletal muscle.
Membrane Cholesterol in Skeletal Muscle: A Novel Player in Excitation-Contraction Coupling and Insulin Resistance
Current evidence supporting an emerging role of cholesterol on excitation-contraction coupling and glucose transport in skeletal muscle is addressed and the increased membrane cholesterol levels displayed by obese animals, which also present insulin resistance, are addressed.


Involvement of dihydropyridine receptors in excitation–contraction coupling in skeletal muscle
It is reported here that low concentrations of a dihydropyridine inhibit charge movements and SR calcium release in parallel, and it is proposed specifically that the molecule that generates charge movement is the dihydopyridine receptor.
Junctional membrane structure and store operated calcium entry in muscle cells.
  • Jianjie Ma, Z. Pan
  • Biology
    Frontiers in bioscience : a journal and virtual library
  • 2003
Results indicate that SOC activation requires an intact interaction between PM and SR, and is linked to conformational changes of ryanodine receptors, and may add to the Ca2+ needed for muscle contraction under conditions of intensive exercise and fatigue.
Sarcoplasmic reticulum contains adenine nucleotide-activated calcium channels
Single-channel recordings of calcium release channels from purified ‘heavy’ SR membranes are reported here on the basis of their activation by adenine nucleotides, blockade by ruthenium red, and selectivity for divalent cations.
Regions of the skeletal muscle dihydropyridine receptor critical for excitation–contraction coupling
The results obtained indicate that the putative cytoplasmic region between repeats II and III of the skeletal muscle DHP receptor3 is an important determinant of skeletal-type EC coupling.
Calcium release from the sarcoplasmic reticulum.
A review of the mechanism of Ca release from the SR of cardiac muscle and this is compared to release in skeletal muscle, and two processes have been proposed as possible links between the action potential of the sarcolemma and the release of Ca from theSR: the Ca-induced release ofCa and the "depolarization-induced"release of Ca.
Ryanodine receptor/Ca2+ release channels and their regulation by endogenous effectors.
Foot structures have been termed feet and are now commonly known as ryanodine receptor/Ca2+ release channels because of the presence of an intrinsic ci+ channel activity within the feet structures, and their ability to bind the plant.
Localization of Ca2+ release channels with ryanodine in junctional terminal cisternae of sarcoplasmic reticulum of fast skeletal muscle.
Direct binding studies with [3H]ryanodine provide evidence on the mode of action of ryanodine and its localization to the terminal cisternae and the low concentration at which the drug is effective appears to account for its toxicity.
Enhanced dihydropyridine receptor channel activity in the presence of ryanodine receptor
The results support the possibility of a retrograde signal by which RyR-1 enhances the function of DHPRs as Ca2+ channels, and measurements of charge movement indicate that the density ofDHPRs is similar in dyspedic and Ry R-1-expressing myotubes.
Physical coupling between ryanodine receptor-calcium release channels.
Regulation of calcium release by interdomain interaction within ryanodine receptors.
It seems that by virtue of such a coordination of the events occurring in various regions of the RyR, the Ca2+ channel can recognize the activation signal received at the cytoplasmic region of theRyR.