nicotinic receptor
Nicotinic receptors are acetylcholine's fast-response switches. Named because nicotine selectively activates them, they are built to react in milliseconds, like a doorbell that immediately opens a gate when pressed rather than passing a message through layers of staff.
They are ligand-gated ion channels: when acetylcholine binds, a central pore opens and lets sodium and other cations flood in, depolarizing the cell almost instantly. Two main types matter pharmacologically: the muscle type at the neuromuscular junction, and the neuronal type in autonomic ganglia and the central nervous system. This is why nicotinic transmission underlies both voluntary muscle movement and the relay through autonomic ganglia.
Two drug classes act here through different mechanisms. Neuromuscular blockers target muscle nicotinic receptors to paralyze skeletal muscle for surgery, while ganglionic blockers target neuronal receptors in ganglia. Both are largely on-off rather than subtle, which makes their effects dramatic and sometimes hazardous.
Rocuronium, a neuromuscular blocker, competes with acetylcholine at muscle nicotinic receptors to relax skeletal muscle and allow a breathing tube to be placed.
Blocking muscle nicotinic receptors for surgery.
Because both sympathetic and parasympathetic ganglia use nicotinic transmission, a ganglionic blocker switches off both branches at once, which is why these drugs cause such widespread and unpredictable effects and are rarely used today.