16.17
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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.