A pharmacology lab tests a toxin that selectively slows the inactivation of voltage-gated Na channels in a single neuron's axon (activation threshold unchanged). During an action potential, Na channels normally inactivate quickly, and delayed rectifier K channels open to repolarize the membrane. The toxin does not affect K channels. Which outcome is most consistent with slowed Na channel inactivation?
Parameters: Na channel inactivation slowed; K channel kinetics unchanged; .
- The action potential duration increases because inward Na current persists longer before repolarization completes. (correct answer)
- Neurotransmitter release decreases because Na channels in the postsynaptic membrane are required for vesicle fusion in the presynaptic terminal.
- The action potential amplitude decreases because prolonged Na channel opening drives the membrane toward instead of .
- Action potentials propagate only toward the soma because delayed Na channel inactivation reverses the direction of current flow along the axon.
Explanation: This question tests understanding of action potential kinetics and the role of Na+ channel inactivation. During a normal action potential, Na+ channels rapidly inactivate after opening, allowing K+ channels to repolarize the membrane. When a toxin slows Na+ channel inactivation, Na+ channels remain open longer, continuing to allow Na+ influx even as K+ channels try to repolarize the membrane. This prolongs the depolarization phase and increases action potential duration. The correct answer (A) accurately describes this prolongation. Answer C incorrectly suggests the amplitude would decrease and that prolonged Na+ opening would drive the membrane toward EK rather than ENa. To analyze channel kinetics problems, consider how changes in channel opening/closing times affect the balance between depolarizing and repolarizing currents.