Linked from

The 50 pages that link to Acetylcholine, each with the reason it gives.

• Autonomic nervous systemRelated: It carries signals at every autonomic ganglion and at parasympathetic target organs.

• Neuromuscular junctionRelated: Motor neurons release it to carry the signal across the synaptic cleft.

• Muscarinic acetylcholine receptorRelated: It is the endogenous ligand that activates every muscarinic receptor subtype.

• AtropineRelated: Atropine prevents acetylcholine from activating muscarinic receptors.

• Organophosphate poisoningRelated: Its excess drives the muscarinic, nicotinic, and central effects of poisoning.

• AcetylcholinesteraseRelated: It is the substrate whose breakdown terminates cholinergic signaling.

• Motor neuronRelated: It carries the motor neuron's chemical message across the neuromuscular junction.

• Parasympathetic nervous systemRelated: Parasympathetic neurons release it at both ganglia and target tissues.

• Nicotinic acetylcholine receptorRelated: Binding acetylcholine opens the receptor’s channel and initiates its response.

• Botulinum toxinRelated: Botulinum toxin prevents its release at neuromuscular junctions.

• Motor unitRelated: It transmits the neuron’s chemical signal across each neuromuscular junction.

• Eccrine sweat glandRelated: Sympathetic nerves chiefly stimulate eccrine secretion using acetylcholine.

• Adrenal medullaRelated: Splanchnic nerve endings release it to excite chromaffin cells.

• PralidoximeRelated: Restored acetylcholinesterase can again break down the acetylcholine that accumulates during poisoning.

• SweatingRelated: Sympathetic nerves stimulate eccrine glands chiefly by releasing acetylcholine.

• BotulismRelated: Botulinum toxin prevents its release from motor nerve endings.

• Cholinergic crisisRelated: Its accumulation or excessive receptor stimulation drives the crisis.

• HyperhidrosisRelated: It is the principal neurotransmitter driving eccrine sweat secretion.

• Acetylcholinesterase inhibitorRelated: Blocking its breakdown increases or prolongs its signaling.

• Nerve agentRelated: Its continued action drives the excessive signaling caused by many nerve agents.

• SarinRelated: Its buildup after sarin exposure overstimulates cholinergic receptors.

• Lower motor neuronRelated: Lower motor neurons release it to trigger muscle-fiber excitation.

• Rapid eye movement sleepRelated: Cholinergic signaling contributes to REM-like cortical activation.

• Bernard KatzRelated: Katz’s best-known release experiments measured acetylcholine transmission to muscle.

• BronchoconstrictionRelated: It transmits parasympathetic signals that can constrict the bronchi.

• Novichok agentsRelated: Its buildup after enzyme inhibition drives the agents’ characteristic overstimulation of nerves.

• NeostigmineRelated: Neostigmine increases its availability rather than binding directly to its receptors.

• DonepezilRelated: Donepezil increases the availability of this neurotransmitter at cholinergic synapses.

• HyoscyamineRelated: Hyoscyamine opposes acetylcholine at muscarinic receptors.

• SomanRelated: Its excess drives the overstimulation caused by soman poisoning.

• Daniel BovetRelated: Bovet also investigated compounds that blocked acetylcholine’s effects.

• Henry Hallett DaleRelated: Dale identified its actions at nerve endings and helped establish it as a neurotransmitter.

• Trigger pointRelated: Excessive release has been proposed as a contributor to persistent muscle contraction at trigger points.

• Bodily secretionsRelated: Parasympathetic acetylcholine signaling stimulates several watery gland secretions.

• Chromaffin SystemRelated: It is released onto chromaffin cells and initiates their secretion.

• MuscarineRelated: Muscarine mimics acetylcholine at muscarinic receptors but is not rapidly broken down by acetylcholinesterase.

• Tetraethyl pyrophosphateRelated: Its buildup after enzyme inhibition drives the compound’s acute effects.

• Urtica dioicaRelated: Acetylcholine is among the compounds detected in nettle stinging hairs.