How would the action potential be affected if these toxins were used?

Question

1.Cyclosarin - inhibits acetylcholinesterase (this is an enzyme that breaks down the neurotransmitter acetylcholine)

2.Saxitoxin - can’t open Na channels

3.Neostigmine - competitively inhibits acetylchoinesterase 

4.Curare - blocks acetylcholine (neurotransmitter) receptors on muscles

5.Botulinum toxin - prevents release of acetylcholine from presynaptic cell

6.Alpha-latroxin (black widow spiders) - causes release of acetylcholine

Answer 1

Hello! In each of these cases, we are presumably discussing a neuromuscular junction - a fancy word for where a neuron meets a muscle cell. There are two things that happen to active a muscle: (1) an action potential propagates down the axon of a motor neuron, and (2) acetylcholine is released into the neuromuscular junction where it activates receptors on the muscle cell causing contraction. Once acetylcholine is released, it must be broken down by an enzyme called acetylcholinesterase to prevent constant contraction. With that information,

1. This inhibits acetylcholinesterase activity. What impact does that have on the action potential?
2. An action potential is propagated by the activity of voltage-gated Na channels. If these can't open, how does that affect the action potential?
3. This is similar to 1.
4. If acetylcholine receptors are blocked, then acetylcholine can be released, but it won't impact the muscle cell. What impact would that have on the action potential?
5. This is similar to 4.
6. This is similar to 1, but with a different mechanism.

I hope this leads you on the right path!