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The sodium–potassium ATPase uses cellular energy to move K + ions inside the cell and Na + ions outside. This alone accumulates a small electrical charge, but a big concentration gradient. There is lots of K + in the cell and lots of Na + outside the cell. Potassium is able to leave the cell through K + channels that are open 90% of the time, and it does. However, Na + channels are rarely open, so Na + remains outside the cell. When K + leaves the cell, obeying its concentration gradient, that effectively leaves a negative charge behind. So at rest, there is a large concentration gradient for Na + to enter the cell, and there is an accumulation of negative charges left behind in the cell. This is the resting membrane potential. Potential in this context means a separation of electrical charge that is capable of doing work. It is measured in volts, just like a battery. However, the transmembrane potential is considerably smaller (0.07 V); therefore, the small value is expressed as millivolts (mV) or 70 mV. Because the inside of a cell is negative compared with the outside, a minus sign signifies the excess of negative charges inside the cell, −70 mV.

If an event changes the permeability of the membrane to Na + ions, they will enter the cell. That will change the voltage. This is an electrical event, called an action potential, that can be used as a cellular signal. Communication occurs between nerves and muscles through neurotransmitters. Neuron action potentials cause the release of neurotransmitters from the synaptic terminal into the synaptic cleft, where they can then diffuse across the synaptic cleft and bind to a receptor molecule on the motor end plate. The motor end plate possesses junctional folds—folds in the sarcolemma that create a large surface area for the neurotransmitter to bind to receptors. The receptors are actually sodium channels that open to allow the passage of Na + into the cell when they receive neurotransmitter signal.

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.

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