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Pharmacology · Autonomic nervous system: nicotine action at ganglia
Sample itemIn a toxicology lecture, nicotine is described as stimulating autonomic ganglia at low doses and blocking them at high doses. What is the basis of the block at high doses?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
D. Persistent depolarisation of the receptor
Nicotine opens the ganglionic nicotinic channel, but at high concentration the membrane stays depolarised and cannot respond, giving a depolarising block. Succinylcholine blocks the motor end plate in a similar way.
Option by option
A. Blockade of choline uptake into the nerve terminal
Blocking choline uptake is the action of hemicholinium, not nicotine.
B. Competitive block of muscarinic receptors
Nicotine acts on nicotinic receptors and has no action as a muscarinic antagonist.
C. Inhibition of acetylcholine synthesis
Nicotine does not interfere with acetylcholine synthesis.
D. Persistent depolarisation of the receptor (correct)
Correct. Prolonged depolarisation makes the ganglion cell unresponsive.
Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.
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