Calcium-induced calcium release (CICR) is a mechanism of calcium release from muscle sarcoplasmic reticulum that was proposed in the 1970s^[1]. Originally proposed for skeletal muscle, subsequent research has revealed that it is actually the predominant mechanism in cardiac muscle.

The muscle cell membrane (sarcolemma) contains many ion receptors. One of which is the voltage-gated ion channel DHPR (Dihydropyridine receptor) which allows the entry of calcium ions into the cytosol - this is the calcium-induced part.

The sarcoplasmic reticulum (myocyte version of the endoplasmic reticulum) stores calcium ions. On the sarcoplasmic reticulum there is a receptor called the Ryanodine Receptor, which is sensitive to cytosolic calcium ions. The Ryanodine receptor is a calcium release channel which releases the sarcoplasmic reticulum's calcium stores - this is the Calcium-release part.

The purpose of this mechanism is to release a very small, yet significant, proportion of calcium into the muscle's cytosol. The calcium ions eventually bind to an accessory protein found on the actin filament, which stimulates muscle contraction.

Ca²⁺ ions are a key component to muscle contraction.

Contents 1 CICR in Excitation-Contraction (EC) Coupling 2 The Paradox of Regenerative Release 3 Termination of CICR 4 References

[edit] CICR in Excitation-Contraction (EC) Coupling

The mechanism that couples excitation - an action potential in the plasma membrane of the muscle cell - and contraction of heart muscle is an increase in the cell's cytosolic calcium concentration. This calcium combines with the regulator protein, troponin, initiating cross-bridge formation between actin and myosin.

[edit] The Paradox of Regenerative Release

[edit] Termination of CICR

[edit] References

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