16.17
Action Potential: Phases of Stimulation
The action potential is a complex electrical event that occurs in excitable cells, such as neurons and muscle cells. It consists of several distinct p…
An action potential has three main phases: depolarization, repolarization, and hyperpolarization.
The depolarizing phase begins after a graded potential or a stimulus triggers the axon membrane to depolarize above a threshold.
This triggers the voltage-gated sodium channels to open rapidly. The resulting influx of sodium ions increases the membrane potential that peaks at +30mV.
Shortly after this, the sodium channels inactivate, preventing further sodium influx. The voltage-gated potassium channels are now open, causing an efflux of potassium ions.
This phase is called the repolarizing phase because the efflux of positive ions decreases the membrane potential.
Due to a slight delay in the closing of the potassium channel, the membrane potential continues past the resting membrane voltage, causing a little dip. This phase is called the hyperpolarization phase.
The action of sodium-potassium ATPase pumps then restores the resting membrane potential.
Once an action potential is generated, the axon cannot initiate another action potential for a brief time known as the refractory period. It ensures the unidirectional flow of nerve impulses and prevents neurons from firing continuously.
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Q1: What triggers the depolarization phase of an action potential?
A graded potential or stimulus causes the axon membrane to depolarize above threshold, triggering voltage-gated sodium channels to open rapidly. Sodium ions flood into the cell, increasing membrane potential to a peak of +30 mV. This positive feedback loop drives further sodium channel opening until channels inactivate.
Q2: Why does the membrane potential become more negative during repolarization?
During repolarization, voltage-gated potassium channels open fully, allowing potassium ions to exit the cell. This efflux of positively charged ions decreases the membrane potential, restoring it toward the resting level of approximately -70 mV. Sodium channels have already inactivated, preventing further sodium influx.
Q3: What causes hyperpolarization and why does it occur?
Hyperpolarization occurs because potassium channels close slightly delayed after the membrane potential returns to resting level. Potassium ions continue exiting the cell briefly, causing the membrane potential to dip below -70 mV to approximately -80 mV. The sodium-potassium ATPase pump then restores the resting membrane potential.
Q4: What is the refractory period and what is its functional significance?
The refractory period is a brief time after an action potential when the axon cannot initiate another action potential. It ensures unidirectional flow of nerve impulses along the axon and prevents neurons from firing continuously. The absolute refractory period prevents any new action potential, while the relative refractory period requires a stronger-than-normal stimulus.
Q5: How do voltage-gated sodium and potassium channels differ in their timing during an action potential?
Voltage-gated sodium channels open rapidly at threshold, allowing quick sodium influx during depolarization. They then inactivate shortly after, stopping sodium entry. Voltage-gated potassium channels open more slowly in response to membrane depolarization and close with a slight delay, extending potassium efflux into the hyperpolarization phase.
Q6: What role does the sodium-potassium ATPase pump play in the action potential cycle?
The sodium-potassium ATPase pump restores the resting membrane potential after hyperpolarization by actively transporting sodium ions out of the cell and potassium ions into the cell. This maintains the ion concentration gradients necessary for repeated action potentials and ensures the neuron can respond to subsequent stimuli.
Q7: How does the sequence of ion channel opening and closing enable unidirectional signal propagation?
The refractory period prevents backward propagation of the action potential along the axon. As depolarization moves forward, the region behind enters the refractory period and cannot fire again. This directional constraint, combined with the coordinated opening and closing of sodium and potassium channels, ensures action potentials propagate in one direction along the neuron.