Question

1. Based on your knowledge of excitation-contraction coupling and the symptoms in this case, what will a cholinesterase inhibitor cause skeletal muscle to do?

2. Based on your knowledge of excitation-contraction coupling and the symptoms in this case, what will a cholinesterase inhibitor cause glands (which also respond to ACh) to do?

3. Based on your knowledge and information provided, what must Atropine be an antagonist for?

Answer 1

1) Cholinesterase inhibitor inhibits the enzyme cholinesterase which functions to digest the acetylcholine. Therefore cholinesterase inhibitors increase the concentration of acetylcholine at the synaptic site by inhibiting its digestion. As acetylcholine levels increase, it will bind repetitively to the nicotinic acetylcholine receptors and end plate potential will be generated which will cross the threshold repetitively and there will be REPETITIVE MUSCLE CONTRACTION leading to fasciculations and twitching. Force of contraction in myasthenic muscles increase. High dose cause persistent depolarization resulting in blockade of neuromuscular transmission which leads to weakness and paralysis.

2) The glands which respond to ACh will become more active as ACh concentration is increased. They will start secreting more. More respiratory secretions, more lacrimal secretions (tears), more intestinal secretions, etc.

3) Atropine is an antagonist of muscarinic cholinergic receptors. It doesn't possess any activity against the nicotinic cholinergic receptors which are present on the skeletal muscle. However, its synthetic substitutes contain little activity but atropine doesn't have any activity against nicotinic receptors. Therefore, paralysis caused by excess of acetylcholine can never be reversed by atropine.