In a laboratory experiment, adding curare, which binds to acetylcholine receptors, to the solution around a muscle decreases the size of the end-plate potential. Adding prostigmine, an acetylcholinesterase blocker, increases the size of the end-plate potential. Explain why.
What will be an ideal response?
By binding to acetylcholine receptors, curare prevents the binding of acetylcholine. Curare does not open the receptor channels. An end-plate potential results from the opening of several ACh receptor channels. Thus, if the receptor is blocked, any end-plate potential that is produced would be smaller. Prostigmine blocks the enzyme that stops ACh action by degrading the neurotransmitter. Interfering with this enzyme prolongs the action of ACh, thus more receptor channels open and the end-plate potential is larger.
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