Neuromuscular junction and autonomic ganglia !

How a nerve makes a skeletal muscle contract, how neuromuscular blockers used in anaesthesia stop it, and what blocking autonomic ganglia does.

Updated 2026-11-01

At the neuromuscular junction, the motor nerve releases acetylcholine onto nicotinic (muscle-type) receptors on the end plate; the muscle depolarises and contracts, and acetylcholinesterase ends the signal. Neuromuscular blockers interrupt this step to relax muscles for intubation and surgery. They come in two kinds, depolarising and non-depolarising, with very different behaviour and risks. Autonomic ganglia use a related, neuronal nicotinic receptor.

Key points

Neuromuscular blockers have no analgesic or sedative effect: they are given only with adequate anaesthesia or sedation, by experienced clinicians, with airway support.
Depolarising (suxamethonium): binds the receptor, depolarises the end plate (fasciculations) and keeps it depolarised; it is broken down by plasma cholinesterase.
Non-depolarising (rocuronium and others): competitive antagonists of acetylcholine at the end plate; reversed by cholinesterase inhibitors (neostigmine) or, for rocuronium and vecuronium, by sugammadex.
Suxamethonium risks: malignant hyperthermia, hyperkalaemia (burns, major trauma, denervation, undiagnosed myopathies in children) and prolonged block with atypical plasma cholinesterase.
Inhaled anaesthetics, aminoglycosides and magnesium enhance non-depolarising block.

Neuromuscular transmission

Nerve action potential opens calcium channels in the terminal
Acetylcholine is released and binds nicotinic receptors on the end plate
Cation entry depolarises the end plate; voltage-gated sodium channels fire a muscle action potential
Acetylcholinesterase in the cleft breaks down acetylcholine so the channel closes

Depolarising versus non-depolarising block

Suxamethonium acts like long-lasting acetylcholine: the end plate depolarises (visible fasciculations) and then cannot respond (phase I block). Giving a cholinesterase inhibitor during phase I deepens the block. With prolonged exposure a phase II block can appear that resembles non-depolarising block. Non-depolarising blockers simply occupy the receptor; more acetylcholine (from neostigmine, given with an antimuscarinic) or removal of the drug (sugammadex binds rocuronium) restores transmission. A nerve stimulator is used to monitor the depth of block.

Safety points

Malignant hyperthermia (RYR1 variants): with volatile anaesthetics or suxamethonium; treated with dantrolene
Hyperkalaemia with suxamethonium after burns, major trauma, denervation or in muscle disease
Atypical or low plasma cholinesterase (genetic, liver disease) prolongs suxamethonium paralysis
Myasthenia gravis: resistant to suxamethonium and very sensitive to non-depolarising blockers
Residual paralysis after surgery: check reversal before removing airway support

Autonomic ganglia

Ganglia use neuronal (NN) nicotinic receptors in both sympathetic and parasympathetic chains. A ganglionic blocker, such as mecamylamine, shuts off both divisions at once, and the effect on each organ is the loss of whichever tone dominated: blood vessels (sympathetic) dilate, causing orthostatic hypotension, while heart (parasympathetic at rest), gut, bladder and eye lose parasympathetic tone, giving tachycardia, constipation, urinary retention and blurred vision. That broad effect is why these drugs are now rarely used.

Test yourself

Think of the answer, then tap the question to see it.

Why must a neuromuscular blocker always be given with sedation or anaesthesia?

It paralyses muscles but has no effect on consciousness or pain, so an awake patient would be paralysed and aware.

What do fasciculations after suxamethonium reflect?

Initial depolarisation of the motor end plates before the block sets in (depolarising, phase I block).

Why does neostigmine not reverse phase I suxamethonium block?

The block is caused by persistent depolarisation; more acetylcholine adds to it, so cholinesterase inhibitors deepen phase I block.

What does a ganglionic blocker do to the heart rate at rest, and why?

It raises it, because at rest the heart is dominated by parasympathetic (vagal) tone, which the blocker removes.

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Educational content on how drugs work; not a prescribing guide and no substitute for a health professional's advice. No doses are given.

Sources: DailyMed - SUCCINYLCHOLINE CHLORIDE injection, solution (DailyMed (U.S. National Library of Medicine), 2026); DailyMed - ROCURONIUM BROMIDE injection, solution (DailyMed (U.S. National Library of Medicine), 2026); 10.2 Skeletal Muscle (OpenStax (Rice University), 2022); 15.4 Drugs that Affect the Autonomic System (OpenStax (Rice University), 2022).

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