14.6:
Generation of Action Potential in Skeletal Muscles
The resting membrane potential of a muscle cell is the difference in electrical charge across its membrane at rest. It is typically around -85 mV.
At a neuromuscular junction, when the acetylcholine released from the axon terminals binds the nicotinic receptors on the motor end plate, it allows sodium ion influx into the muscle fiber.
This influx makes the membrane potential less negative, leading to local depolarization at the motor end plate.
If this potential change crosses a threshold of -50 to -55 mV, it opens voltage-gated sodium channels, triggering an action potential — a self-propagating electrical signal.
The action potential starts a depolarization wave by opening adjacent voltage-gated sodium ion channels, propagating the signal along the entire muscle fiber.
After the depolarization of the membrane reaches its highest point of about +40 mV, also known as the overshoot, the voltage-gated sodium channels shut down.
Simultaneously, the overshoot potential opens the voltage-gated potassium channels for the exit of potassium ions, dropping the electric charge of the membrane back to its resting potential. This phase is called repolarization.
14.6:
Generation of Action Potential in Skeletal Muscles
Every cell in the body maintains a membrane potential due to an uneven distribution of positive and negative charges across its plasma membrane. The membrane potential is measured in millivolts and quantifies the difference in charge across the membrane.
Like neurons, muscle cells are also regarded as excitable due to their capacity to change in response to stimuli, primarily due to voltage-gated ion channels embedded in their plasma membranes, which get activated by alterations in the cell's membrane potential.
In the resting state, a muscle cell maintains a negative internal charge called the resting membrane potential. The activity of the sodium-potassium pumps, which actively move potassium ions into the cell and sodium ions out of the cell, is instrumental in setting up the resting membrane potential. However, when a muscle cell receives a chemical signal at a neuromuscular junction, it triggers the opening of chemically-gated sodium channels. Sodium ions rush into the cell because of the concentration and electrical gradient, causing a localized depolarization — a scenario where the cell's inside becomes less negative.
In the event of this depolarization reaching a threshold, it opens voltage-gated sodium channels, resulting in a rapid influx of more sodium ions into the cell. This event generates a full-blown action potential, where the internal charge of the cell momentarily becomes positive, reaching a point called the overshoot.
Following this peak, voltage-gated potassium channels open to allow potassium ions to leave the cell, bringing about repolarization where the internal charge returns to its resting negative state. This entire event, from the initial depolarization to the subsequent repolarization, represents one complete action potential.
In conclusion, the excitability of muscle cells is a dynamic and complex process that carefully orchestrates ion movements across the cell membrane. This sequence enables the muscle cell to swiftly respond to signals, effectively transmit electrical impulses, and ultimately facilitate bodily movements.