Summary of Biochemical Events of Muscle Contraction
1. Nerve impulse arrives at neuromuscular junction (neuron to muscle cell communication). 2. Acetylcholine (ACh) is released from motor neuron and diffuses across to the motor end plate. 3. ACh binds with nicotinic receptors at the motor end plate (a specialized portion of sarcolemma). Receptors are linked to ligand gated ion channels, allowing Na+ influx (plus a little bit of K+ efflux), resulting in the depolarization of the muscle cell membrane. This results in a motor end plate potential, which becomes an action potential (AP) in muscle cells. 4. The impulse (AP) is spread very quickly through out the cell by the transverse ("T") tubules. Located on the T-tubules are the dihydropyridine (DHP) receptors that are mechanically linked to the lateral sacs (terminal cisternae) of the sarcoplasmic reticulum (SR). When triggered by the change in membrane potential (AP) traveling down the t-tubules, the DHP receptors mechanically opens gates on the SR. This then causes the SR to release the Ca2+ it has stored there into the cytosol (sarcoplasm) of the skeletal muscle. 5. The increase in [Ca2+]i binds to the regulatory protein troponin, causing it to change shape and move. 6. The movement of troponin then moves tropomyosin away from covering the active site on actin, thus exposing the myosin binding site on actin.This muscle contraction will continue until: 1) the impulse stops or 2) fatigue occurs.
If Nerve Impulse Stops:
1. Ca2+ will be pumped back into SR (re-sequestered) by active transport (Ca2+ATPase). 2. Without the increased [Ca2+]i, troponin is no longer bound to Ca2+and the tropomyosin then moves back over to cover the binding sites on actin. Thus crossbridges formation cannot occur. 3. When all the myosin heads detach, actin slides back to its original position and the muscle relaxes.