Question

1. What would happen if there were a blockage to voltage-gated Na⁺ channels during an action potential?

2. What would occur to an action potential if there was delayed inactivation of voltage-gated Na⁺ channels?

3. What would happen to an action potential when a toxin prevents ACh binding to nAChRs on muscle fibres?

4. What would happen to an action potential if a toxin which forms pores in the cell membrane of neurons, allowing the influx of Ca²⁺ into the nerve terminal

Answer 1

If there is blockage of voltage gated Na+ channels - then there would be no Na+ influx ---> so no depolarization----> no action potential.

2, for another action potential to set in, there should be repolarization after depolarization...if there is delayed inactivation of Na+ channel, then no repolarization occurs and hence no another action potential sets in.

3, the toxin which prevents binding of Ach to its receptor causes skeletal muscle paralysis. The mechanism of action is the toxin has antagonist action at the nicotinic receptors.

4, Ca2+ in the membrane causes vesicles with Ach to fuse with the pre synaptic membrane and favour the release of Ach. So increased Ca2+ in the pre synaptic terminal causes increased force of contraction.