As sodium channels inactivate, which flow drives the falling phase of this neuronal spike?

• Sodium entering through rapidly activated channels
• Potassium entering through membrane pumps
• Potassium leaving through delayed channels

In the sodium-based neuronal spike described here, what drives the rapid rising phase?

• Potassium entering through leak channels
• Sodium entering through fast channels
• Sodium leaving through membrane pumps

At threshold in this sodium-based spike, sodium entry depolarizes the membrane and opens more sodium channels, making the rise self-amplifying.

Why can this neuron not produce a second spike during its absolute refractory period?

• Potassium inside the axon falls to zero
• Too few sodium channels are available to open
• Sodium-potassium pumps pause until the membrane cools

How does an inactivated sodium channel differ from a closed-available sodium channel?

• It passes sodium while still inactivated
• It can reopen immediately if depolarized
• It must recover before it can open again

Once membrane-charging current is accounted for, what can a voltage-clamp recording reveal before individual ionic currents are isolated?

• Separate sodium and potassium currents without other tests
• Net ionic current at the chosen membrane voltage
• The exact number of sodium channels in each cell

During the relative refractory period, some sodium channels have recovered but potassium conductance is still high. What is usually needed to trigger another spike?

• A stronger depolarizing stimulus
• A much weaker depolarizing input
• A pump reversing ionic gradients

In this spike model, a blocker reduces delayed potassium current. Sodium-channel function and ion gradients stay unchanged. What is the expected effect on repolarization?

• Sodium entry stops, so the rise stops
• The return toward resting voltage becomes slower
• The potassium equilibrium voltage instantly reverses