The sequence of events that converts action potentials in a muscle fiber to a contraction is know as excitation contraction coupling. In order for a skeletal muscle fiber to contract, it has to get a signal from the nervous system. The part of the nervous system that it gets a signal from is called a motor neuron. An electoral signal, called an action potential travels down the axon and to the axon terminal. At the end of the motor neuron are structures called synaptic vesicles and they contain different neurotransmitters. In the case of a motor neuron that stimulates a skeletal muscle fiber, that neurotransmitter is called acetylcholine.
When the action potential gets down to the end it will cause the synaptic vesicles to release acetylcholine. The ACH crosses the synapse, which is a physical gap between the motor neuron and the muscle fiber and binds to ACH receptors. A flowing in of sodium (Na+) and a flowing out of potassium (K+) results which, depolarizes the cell and generates an end-plate potential. This causes a depolarizing excitatory postsynaptic potential (EPSP). The opposite of this is called, inhibitory postsynaptic potential (IPSP), which usually result from the flow of negative ions in and positive ions out of a cell.
If enough ACH neurotransmitters bind to receptors, it induces an action potential in the muscle fiber and that will induce the muscle fiber to release calcium (Ca2+) from the sarcoplasmic reticulum. An action potential travels across the entire sarcolemma and is rapidly conducted into the interior of the muscle fiber by structures called t-tubules. The t-tubules make contact with the Ca2+ filled sarcoplasmic reticulum. The Ca2+ released from the sarcoplasmic reticulum binds to troponin complex by the actin filaments, which causes the troponin complex to pull tropomyosin away.
Because these chemicals have a high affinity for calcium ions they cause the myosin cross-bridges to attach to actin and flex rapidly. We also must remember that adenosine triphosphate (ATP) has to get broken down and by breaking it down, it allows the myosin cross-bridge to power stroke by consuming the energy that the ATP gives off. Once the signal from the motor neuron stops, no more ACH binds onto the receptors, which causes the Ca2+ to be transported back into the sarcoplasmic reticulum. Without the calcium, the active site is closed and myosin can no longer bind and the sarcomere goes back to its resting length.
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