Excitation-contraction coupling
Introduction
Excitation-contraction (EC) coupling is a term coined in 1952 to describe the physiological process of converting an electrical stimulus to mechanical response [1]. This process is fundamental to muscle physiology, whereby the electrical stimulus is usually an action potential and the mechanical response is contraction. EC coupling can be dysregulated in many disease conditions.
Though EC coupling has been known for over half a century, it is still an active area of biomedical research. The general scheme is that an action potential arrives to depolarise the cell membrane. By mechanisms specific to the muscle type, this depolarisation results in an increase in cytosolic calcium that is called a calcium transient. This increase in calcium activates calcium-sensitive contractile proteins that then use ATP to cause cell shortening.
Skeletal Muscle
1. Acetylcholine released by axon of motor neuron crosses cleft and binds to receptors/channels on motor end plate
2. Action potential generated in response to binding of acetylcholine and subsequent end plate potential is propagated across surface membrane and down T tubules of muscle cell
3. Action potential in T tubule triggers Ca2+ (calcium) release from sarcoplasmic reticulum
4. Calcium ions released from lateral sacs bind to troponin on actin filaments; leads to tropomyosin being physically moved aside to uncover cross-bridge binding sites on actin
5. Myosin cross bridges attach to actin and bend, pulling actin filaments toward center of sarcomere; powered by energy provided by ATP
6. Ca2+ actively taken up by sarcoplasmic reticulum when there is no longer local action potential
7. With Ca2+ no longer bound to troponin, tropomyosin slips back to its blocking position over binding sites on actin; contraction ends; actin slides back to original resting position
Cardiac Muscle
