If a mutation caused a neuron to have twice as many open "leak" potassium channels (ungated channels) as a normal neuron, how would the resting membrane potential be affected?

Question

If a mutation caused a neuron to have twice as many open "leak" potassium channels (ungated channels) as a normal neuron, how would the resting membrane potential be affected?

BlackTom AI · Accepted Answer

Question restatement: If a mutation caused a neuron to have twice as many open leak potassium channels (ungated) as a normal neuron, how would the resting membrane potential be affected?

Option 1: It would be closer to the sodium equilibrium potential (+62 mV).
- This is unlikely because increasing open leak channels for potassium drives the membrane potential toward the potassium equilibrium potential, not toward the sodium equilibrium potential. Potassium equilibrium potential is typically negative, and with more K+ leak, the cell becomes more negative, not closer to +62 mV.

Option 2: It would be less negative (e.g., -50 mV) because potassium would enter the cell.
- This contradicts the basic electrochemical gradient for potassium. Potassium tends to exit the cell when leak channels are open, not enter. If K+ moved into the cell, that would tend to depolarize the membrane, but the leak conductance favors K+ efflux, making the inside more negative. So this option misstates the direction of K+ movement and the resulting effect on membrane potential.

Option 3: It would not change because leak channels do not affect resting potential.
- This is incorrect. Leak channels, especially for K+, are critical in setting the resting membrane potential. Opening more K+ leak channels increases K+ permeability, which drives the membrane potential toward the K+ equilibrium potential. Therefore, the resting potential would change.

Option 4: It would be more negative (e.g., -80 mV or -90 mV) because more potassium would leave the cell.
- This aligns with the fundamental principle that increasing potassium leak conductance increases K+ efflux, which hyperpolarizes the cell (makes the inside more negative) toward the K+ equilibrium potential. The numerical examples provided (-80 to -90 mV) are within the typical range for a hyperpolarized resting potential in neurons under increased K+ permeability. The logic here correctly identifies both the direction of K+ movement and the consequent shift in membrane potential.

Summary reasoning: Potassium leak channels set the resting potential by allowing K+ to move according to its concentration gradient. Doubling their number increases K+ permeability, prompting more K+ to exit the cell, which makes the inside more negative and moves the resting potential closer to the K+ equilibrium potential. The other options either misstate the direction of potassium movement, misattribute the effect to sodium potential, deny the role of leak channels, or claim no change, all of which contradict established membrane physiology.

Bio 93 Section CDE 2025 Final- Section E

If a mutation caused a neuron to have twice as many open "leak" potassium channels (ungated channels) as a normal neuron, how would the resting membrane potential be affected?

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