A toxin selectively and completely blocks voltage-gated K⁺ channels without affecting voltage-gated Na⁺ channels. What effect would this have on neuronal action potentials?
ADepolarization would be blocked because K⁺ influx normally drives the rising phase of the action potential
BAction potentials would be broader and prolonged, with repolarization severely impaired or absent
CThe resting membrane potential would immediately become more positive due to loss of K⁺ permeability
DNa⁺ channels would fail to open because they require K⁺ channel co-activation
Voltage-gated K⁺ channels are responsible for repolarization — their opening drives K⁺ out of the cell, rapidly restoring the negative membrane potential. If they are blocked, the depolarization caused by Na⁺ influx cannot be reversed efficiently, causing the action potential to broaden dramatically or plateau. Option A reverses the ionic flows: Na⁺ (not K⁺) drives depolarization. Option C is wrong because voltage-gated K⁺ channels are largely closed at rest — resting potential is set by constitutive leak channels, not voltage-gated ones.
Question 2 Multiple Choice
What is the primary reason voltage-gated K⁺ channels cause afterhyperpolarization — a brief dip in membrane voltage below the resting potential?
AThey lack fast inactivation, so they continue conducting K⁺ outward even after the membrane passes through the resting potential, pulling voltage below rest
BThey have a fast inactivation gate that closes precisely at -70 mV, causing a brief overshoot below rest
CK⁺ rushes inward at negative voltages, hyperpolarizing the cell below its equilibrium potential
DNa⁺ channels reopen at voltages below -70 mV, producing an inward current that causes undershoot
Voltage-gated K⁺ channels lack the fast inactivation gate that Na⁺ channels possess. They stay open as long as the membrane is depolarized. As repolarization proceeds and the membrane voltage drops back through -70 mV toward the K⁺ equilibrium potential (~-90 mV), the channels are still open and still conducting K⁺ outward, continuing to pull the voltage more negative. Only once the membrane is sufficiently negative do the channels slowly close, allowing the resting potential to be re-established. Option B is wrong because K⁺ channels lack fast inactivation entirely — this is a defining feature distinguishing them from Na⁺ channels.
Question 3 True / False
The delay in voltage-gated K⁺ channel opening relative to Na⁺ channel opening is essential for the action potential to reach its positive peak before repolarization begins.
TTrue
FFalse
Answer: True
If K⁺ channels opened as rapidly as Na⁺ channels, K⁺ efflux would immediately counteract Na⁺ influx, preventing the membrane from depolarizing to its characteristic peak near +30 mV. The delayed opening means that the Na⁺ channels have time to drive the membrane strongly positive before K⁺ channels begin their repolarizing current. This timing is not accidental — it results from the slower conformational rearrangement required to open K⁺ channel pores.
Question 4 True / False
Like voltage-gated Na⁺ channels, voltage-gated K⁺ channels possess a fast inactivation gate that closes the channel within milliseconds of opening, regardless of membrane voltage.
TTrue
FFalse
Answer: False
This is the key structural difference between the two channel types. Voltage-gated Na⁺ channels have a fast inactivation mechanism (the 'ball and chain' inactivation gate) that closes the channel within ~1 ms of opening, independent of whether the membrane is still depolarized. Voltage-gated K⁺ channels (delayed rectifiers) lack this fast inactivation gate — they remain open as long as the membrane stays depolarized. This difference is what causes afterhyperpolarization and makes K⁺ channels the primary determinant of action potential duration.
Question 5 Short Answer
Why do voltage-gated K⁺ channels cause afterhyperpolarization, and what does this reveal about their gating mechanism compared to voltage-gated Na⁺ channels?
Think about your answer, then reveal below.
Model answer: Afterhyperpolarization occurs because voltage-gated K⁺ channels lack fast inactivation. Na⁺ channels have an inactivation gate that closes the channel within ~1 ms of opening regardless of membrane voltage, automatically terminating Na⁺ influx. K⁺ channels have no equivalent mechanism — they stay open as long as the membrane remains depolarized. As repolarization proceeds and the voltage passes through -70 mV, K⁺ channels are still open and still driving K⁺ outward toward the ~-90 mV equilibrium potential, pulling the voltage below rest. Only when the membrane becomes sufficiently negative do the channels finally close, allowing leak channels to restore the resting potential. The afterhyperpolarization is therefore a direct consequence of K⁺ channels' inability to self-terminate — their open duration is set by the voltage, not by an intrinsic timer.
This question tests whether students understand that the gating properties of K⁺ channels — specifically the absence of fast inactivation — have direct functional consequences for action potential shape. Students who know only that 'K⁺ channels repolarize the membrane' without understanding this distinction cannot explain why the membrane briefly overshoots below rest.