Which ion movement drives repolarization and subsequent hyperpolarization during an action potential?

Which ion movement drives repolarization and subsequent hyperpolarization during an action potential?

• A. Sodium influx through voltage-gated Na+ channels
• B. Calcium influx through voltage-gated Ca2+ channels
• C. Potassium efflux through voltage-gated K+ channels
• D. Chloride influx through ligand-gated channels

Answer: (C)

Repolarization and the following hyperpolarization are driven by potassium leaving the cell through voltage-gated potassium channels. After the rapid depolarization, the sodium channels inactivate and potassium channels open, allowing K+ to flow out. This outward current lowers the internal positivity, pulling the membrane potential back toward the resting level. The potassium channels stay open a bit longer, so more K+ exits than is needed to simply return to rest, causing a brief hyperpolarization below the resting potential. Eventually these channels close and the membrane potential returns to baseline. Sodium influx through voltage-gated Na+ channels drives the initial rise in membrane potential, not the repolarization. Calcium influx through voltage-gated Ca2+ channels can shape depolarization or create a plateau in certain cells, but it is not the main driver of repolarization. Chloride influx through ligand-gated channels is more associated with inhibitory signaling rather than the fast repolarization phase of an action potential.

Repolarization and the following hyperpolarization are driven by potassium leaving the cell through voltage-gated potassium channels. After the rapid depolarization, the sodium channels inactivate and potassium channels open, allowing K+ to flow out. This outward current lowers the internal positivity, pulling the membrane potential back toward the resting level. The potassium channels stay open a bit longer, so more K+ exits than is needed to simply return to rest, causing a brief hyperpolarization below the resting potential. Eventually these channels close and the membrane potential returns to baseline.

Sodium influx through voltage-gated Na+ channels drives the initial rise in membrane potential, not the repolarization. Calcium influx through voltage-gated Ca2+ channels can shape depolarization or create a plateau in certain cells, but it is not the main driver of repolarization. Chloride influx through ligand-gated channels is more associated with inhibitory signaling rather than the fast repolarization phase of an action potential.