 In this video, I will describe the structure of the neuromuscular junction and the mechanism of excitation contraction coupling. The neuromuscular junction is a synapse between a somatic motor neuron and a skeletal muscle fiber. The neuromuscular junction consists of the axon terminal, which is the end of the motor neuron that releases neurotransmitters to excite the skeletal muscle fiber. The name of that neurotransmitter is acetylcholine, abbreviated ACH in the illustration here. Then the motor end plate is the region of the muscle fiber, the sarcolemma surface that contains the neurotransmitter receptors. These receptors are ion channels that will be activated by acetylcholine, they're known as nicotinic acetylcholine receptors. So the motor end plate is the plasma membrane, the sarcolemma of the skeletal muscle fiber and the axon terminal is the end of the motor neuron releasing neurotransmitter. The space that separates the axon terminal from the motor end plate at the neuromuscular junction is known as the synaptic cleft. So the synaptic cleft is a small space between the axon terminal and the motor end plate where the neurotransmitter acetylcholine is released, then acetylcholine will diffuse across the synaptic cleft and bind to the nicotinic acetylcholine receptors at the motor end plate. A motor unit is an individual motor neuron and all of the muscle fibers that that motor neuron excites. So one motor neuron's axon could branch to form multiple neuromuscular junctions and when an action potential travels down the axon of a motor neuron it will stimulate contraction of all of the muscle fibers in that motor unit. The mechanism of excitation contraction coupling is initiated with the release of acetylcholine from the somatic motor neuron's axon terminal, acetylcholine diffuses across the synaptic cleft and binds to the nicotinic acetylcholine receptors on the motor end plate. These nicotinic acetylcholine receptors are ion channels that open allowing sodium ions to enter the cell and these as this occurs it will stimulate an action potential by activating voltage gated ion channels. And this action potential is an electrical impulse that spreads through the skeletal muscle fiber traveling along the sarcolemma as ions rush in and out of the skeletal muscle fiber across the sarcolemma. This is why the transverse tubules are important to help the action potential travel deep within the skeletal muscle fiber. The action potential will activate the voltage gated calcium channels in the sarcoplasmic reticulum and the terminal cisternae of the sarcoplasmic reticulum are adjacent to the transverse tubules therefore that's the location that will become activated to release calcium. So calcium moves from the sarcoplasmic reticulum out into the cytoplasm of the muscle fiber and calcium is the mediator of excitation contraction coupling. So the excitation that started off with the neurotransmitter producing an action potential in the muscle fiber and that stimulates the sarcoplasmic reticulum to release calcium then the calcium will stimulate the myofibrils to enter the contraction mechanism. So calcium will bind to a calcium sensor protein known as troponin within the thin myofilaments. This will cause the movement of tropomyosin which exposes binding sites of actin for myosin to bind to then myosin will perform the power stroke cycle creating the movement that causes the muscle to shorten and produces muscle tension. Here we see the structure of the myofilaments in the sarcomere. The thick myofilaments are made of the motor protein myosin ATPase whereas the thin myofilaments consist of actin as well as tropomyosin and the calcium sensor protein troponin. The actin proteins each have a binding site for myosin. The myosin head will bind to that site on actin however tropomyosin is covering the binding site for myosin on actin in the thin filaments when the muscle fiber is at rest. During excitation calcium will bind to troponin and troponin will change shape causing tropomyosin to move and tropomyosin moves off of the binding site for myosin on actin and this will enable myosin heads to bind to actin the first step of the power stroke cycle the cross bridge formation the first step of the power stroke cycle is cross bridge formation where the myosin head binds to actin the second step of the power stroke cycle is the working stroke or power stroke when the myosin head pivots and pulls the actin filament toward the M line of the sarcomere the third step of the power stroke cycle is cross bridge detachment where the ATP molecule will bind to the myosin head stimulating the myosin to release from the actin in the fourth step of the power stroke cycle cocking of the myosin head is when the myosin ATPase will catalyze hydrolysis of ATP to form ADP and phosphate a large amount of energy is released as ATP is broken down into ADP and phosphate and that energy is converted into the potential energy that is stored in the myosin head in the high energy or cocked shape the fourth step then prepares for the first step because this is a cycle at the end of cocking of the myosin head the myosin head is energized and ready to begin another power stroke cycle with cross bridge formation and another working stroke as the cross bridge cycle progresses myosin pulls actin so that the thin filaments overlap more with thick filaments the eye band of the sarcomere will decrease as the overall length of the sarcomere shortens as contraction progresses as long as calcium is bound to troponin the power stroke cycle mechanism can continue as long as there's enough ATP to keep fueling the power stroke cycle so muscle relaxation occurs when calcium is pumped back into the sarcoplasmic reticulum which will then cause troponin to change its shape and triple myosin to move back onto the binding sites for myosin of actin this will prevent cross bridge formation and allow the muscle to relax