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Acetylcholine (ACh) is a neurotransmitter released by motor neurons that binds to receptors in the motor end plate. Neurotransmitter release occurs when an action potential travels down the motor neuron’s axon, resulting in altered permeability of the synaptic terminal membrane and an influx of calcium. The Ca 2+ ions allow synaptic vesicles to move to and bind with the presynaptic membrane (on the neuron), and release neurotransmitter from the vesicles into the synaptic cleft. Once released by the synaptic terminal, ACh diffuses across the synaptic cleft to the motor end plate, where it binds with ACh receptors. As a neurotransmitter binds, these ion channels open, and Na + ions cross the membrane into the muscle cell. This reduces the voltage difference between the inside and outside of the cell, which is called depolarization. As ACh binds at the motor end plate, this depolarization is called an end-plate potential. The depolarization then spreads along the sarcolemma, creating an action potential as sodium channels adjacent to the initial depolarization site sense the change in voltage and open. The action potential moves across the entire cell, creating a wave of depolarization.

ACh is broken down by the enzyme acetylcholinesterase    (AChE) into acetyl and choline. AChE resides in the synaptic cleft, breaking down ACh so that it does not remain bound to ACh receptors, which would cause unwanted extended muscle contraction ( [link] ).

Art connection

There are four steps in the start of a muscle contraction. Step 1: Acetylcholine released from synaptic vesicles in the axon terminal binds to receptors on the muscle cell plasma membrane. Step 2: An action potential is initiated that travels down the T tubule. Step 3: Calcium ions are released from the sarcoplasmic reticulum in response to the change in voltage. Step 4: Calcium ions bind to troponin, exposing active sites on actin. Cross-bridge formation occurs and muscles contract. Three additional steps are part of the end of a muscle contraction. Step 5: Acetylcholine is removed from the synaptic cleft by acetylcholinesterase. Step 6: Calcium ions are transported back into the sarcoplasmic reticulum. Step 7: Tropomyosin covers active sites on actin preventing cross-bridge formation, so the muscle contraction ends.
This diagram shows excitation-contraction coupling in a skeletal muscle contraction and contains details not included in the text. Therefore, it is essential that you read it carefully and study each step. The sarcoplasmic reticulum (SR) is a specialized endoplasmic reticulum found in muscle cells that stores calcium ions. The action potential within skeletal muscle travels down the T (Transverse) tubules and triggers the release of calcium ions from the SR. The calcium ions bind with troponin/tropomyosin to uncover the myosin binding sites so that contraction can occur.

After depolarization, the membrane returns to its resting state. This is called repolarization, during which voltage-gated sodium channels close. Potassium channels continue at 90% conductance. Because the plasma membrane sodium–potassium ATPase always transports ions, the resting state (negatively charged inside relative to the outside) is restored. The period immediately following the transmission of an impulse in a nerve or muscle, in which a neuron or muscle cell regains its ability to transmit another impulse, is called the refractory period. During the refractory period, the membrane cannot generate another action potential. . The refractory period allows the voltage-sensitive ion channels to return to their resting configurations. The sodium potassium ATPase continually moves Na + back out of the cell and K + back into the cell, and the K + leaks out leaving negative charge behind. Very quickly, the membrane repolarizes, so that it can again be depolarized.

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Source:  OpenStax, Human biology. OpenStax CNX. Dec 01, 2015 Download for free at http://legacy.cnx.org/content/col11903/1.3
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