Question

The nicotinic acetylcholine receptor is an ionotropic receptor that can be activated by nicotine, a stimulant drug found in cigarettes. Additionally, alpha-bungarotoxin, a neurotoxin found in the venom of some snakes, binds preferentially & tightly to the closed conformation of the receptors. Another drug, donepezil, is a potent acetylcholinesterase inhibitor used to treat patients w/ Alzheimer's disease. If applied at a neuromuscular junction, indicate whether each of the compounds 1. acetylcholine, 2. nicotine, & 3. alpha-bungarotoxin, & 4. donepezil would enhance (E) or suppress (S) the Ca²⁺ influx in muscle cells.

Answer 1

Acetylcholine and nicotine enhance Ca²⁺ influx at the neuromuscular junction by activating the nicotinic acetylcholine receptor, while alpha-bungarotoxin suppresses it by binding to the receptor in a closed state. Donepezil enhances Ca²⁺ influx indirectly by inhibiting acetylcholinesterase, thereby increasing acetylcholine levels and receptor activation.

Step-by-step explanation:

The nicotinic acetylcholine receptor is an ionotropic receptor found in neuromuscular junctions (NMJ) and is activated by the endogenous neurotransmitter acetylcholine as well as exogenous substances like nicotine.

When considering the effects of various compounds on the Ca²⁺ influx in muscle cells at a neuromuscular junction:

1. Acetylcholine (E) - As the natural ligand for nicotinic receptors, acetylcholine will enhance the calcium influx by causing the receptors to open their associated ion channels.
2. Nicotine (E) - A stimulant found in cigarettes, nicotine will also bind to the nicotinic receptors and enhance calcium influx by mimicking acetylcholine's effect on the receptor.
3. Alpha-bungarotoxin (S) - A neurotoxin that binds tightly to the closed conformation of nicotinic receptors, alpha-bungarotoxin suppresses calcium influx by blocking receptor activation and preventing ion channel opening.
4. Donepezil (E) - While donepezil does not directly interact with the nicotinic receptor, it is a potent inhibitor of acetylcholinesterase, the enzyme that degrades acetylcholine. By preventing the breakdown of acetylcholine, donepezil indirectly enhances calcium influx through prolonged activation of the nicotinic receptors.