Acetylcholine release at cholinergic neuron

Acetylcholine release at cholinergic sympathetic and parasympathetic neurons refers to the biological process by which the neurotransmitter acetylcholine is released from nerve terminals of cholinergic neurons in both the sympathetic and parasympathetic branches of the autonomic nervous system. This is not a single molecular target such as a receptor or enzyme, but rather a physiological event involving multiple proteins including choline acetyltransferase for synthesis, vesicular transporters for storage, SNARE proteins for vesicle fusion, and voltage-gated calcium channels for triggering exocytosis[1][2][3]. In this process, acetylcholine is synthesized from choline and acetyl-CoA by choline acetyltransferase within presynaptic neurons. Upon arrival of an action potential at the nerve terminal, calcium influx triggers synaptic vesicles containing acetylcholine to fuse with the plasma membrane—releasing their contents into the synaptic cleft. The released acetylcholine then binds to postsynaptic muscarinic or nicotinic receptors on target cells to mediate various physiological effects such as muscle contraction or modulation of organ function[1][2][5]. The action of acetylcholine is rapidly terminated by enzymatic breakdown via acetylcholinesterase[2][5]. This entry does not refer to a specific druggable protein target but rather describes a general neurophysiological mechanism; therefore it should not be considered a canonical therapeutic target itself. However, several drugs act on components involved in this process—for example botulinum toxin inhibits vesicle fusion preventing ACh release while black widow spider venom causes excessive ACh exocytosis leading to overstimulation[3]. Disruption in this pathway can contribute to diseases like myasthenia gravis or neurodegenerative conditions where cholinergic signaling is impaired. > "Acetylcholine is synthesized from choline and acetyl-CoA via choline acetyltransferase... transported into vesicles and released into the synaptic cleft... where it can bind muscarinic/nicotinic receptors"[1]. > > "The release of ACh occurs through Ca²⁺ stimulated docking... Many toxins are known that interfere with these processes..."[3]. Because this term describes an event/process—not an individual molecule—it should be flagged as incorrect if used as a molecular drug target.

Other names

Cholinergic neurotransmissionACh releaseCholinergic synaptic transmission

Inhibition of vesicular fusion and neurotransmitter exocytosis (botulinum toxin)