In: Anatomy and Physiology
In muscle contraction, the presynaptic motor neuron releases neurotransmitter in response to action potential generation in axon hillock via synaptic vesicle fusion. The acetylcholine released binds to the receptors on sarcolemma of muscle cell. This results in action potential being transduced to the T tubule. The T tubules have L type calcium channels that cause flow of calcium ions into the cell. The calcium ions then activate the ryanodine receptors which then cause influx of calcium from terminal cisternae of the sarcoplasmic reticulum (SR) into the cytoplasm. The terminal cisternae are stores of calcium in SR. The calcium ions then bind to troponin. Troponin is bound to trophomyosin which masks the myosin binding sites on actin. Binding of troponin to calcium, cause shift in trophomyosin. As a result, the myosin binding sites on actin are released. Myosin can now bind to actin and cross bridging can occur leading to power stroke and muscle contraction.
If calcium is not present in the cytoplasm, or cannot be released from to SR to cytoplasm, it cannot bind to troponin. Hence, trophomyosin will still mask the myosin binding sites on actin. Hence, myosin cannot bind actin. This prevents the cross bridging and will inhibit muscle contraction.