Acetylcholine - wikipedia Acetylcholine Not to be confused with Acetyl chloride. Acetylcholine Clinical data Synonyms ACh Physiological data Source tissues motor neurons, parasympathetic nervous system, brain Target tissues skeletal muscles, brain, many other organs Receptors nicotinic, muscarinic Agonists nicotine, muscarine, cholinesterase inhibitors Antagonists tubocurarine, atropine Precursor choline, acetyl - CoA Biosynthesis choline acetyltransferase Metabolism acetylcholinesterase Identifiers IUPAC name 2 - Acetoxy - N, N, N - trimethylethanaminium CAS Number 51 - 84 - 3 PubChem CID 187 IUPHAR / BPS 294 DrugBank EXPT00412 ChemSpider 182 KEGG C01996 E number E1001 ( i ) ( additional chemicals ) ECHA InfoCard 100.000. 118 Acetylcholine ( ACh ) is an organic chemical that functions in the brain and body of many types of animals, including humans, as a neurotransmitter -- a chemical released by nerve cells to send signals to other cells. Its name is derived from its chemical structure : it is an ester of acetic acid and choline. Parts in the body that use or are affected by acetylcholine are referred to as cholinergic. Substances that interfere with acetylcholine activity are called anticholinergics. Acetylcholine is the neurotransmitter used at the neuromuscular junction -- in other words, it is the chemical that motor neurons of the nervous system release in order to activate muscles. This property means that drugs that affect cholinergic systems can have very dangerous effects ranging from paralysis to convulsions. Acetylcholine is also used as a neurotransmitter in the autonomic nervous system, both as an internal transmitter for the sympathetic nervous system and as the final product released by the parasympathetic nervous system. In the brain, acetylcholine functions as a neurotransmitter and as a neuromodulator. The brain contains a number of cholinergic areas, each with distinct functions. They play an important role in arousal, attention, memory and motivation. Partly because of its muscle - activating function, but also because of its functions in the autonomic nervous system and brain, a large number of important drugs exert their effects by altering cholinergic transmission. Numerous venoms and toxins produced by plants, animals, and bacteria, as well as chemical nerve agents such as Sarin, cause harm by inactivating or hyperactivating muscles via their influences on the neuromuscular junction. Drugs that act on muscarinic acetylcholine receptors, such as atropine, can be poisonous in large quantities, but in smaller doses they are commonly used to treat certain heart conditions and eye problems. Scopolamine, which acts mainly on muscarinic receptors in the brain, can cause delirium and amnesia. The addictive qualities of nicotine are derived from its effects on nicotinic acetylcholine receptors in the brain. Contents 1 Chemistry 2 Biochemistry 3 Functions 3.1 Cellular effects 3.2 Neuromuscular junction 3.3 Autonomic nervous system 3.3. 1 Direct Vascular Effects 3.4 Central nervous system 3.4. 1 Memory 4 Diseases and disorders 4.1 Myasthenia gravis 5 Pharmacology 5.1 Nicotine 5.2 Atropine 5.3 Cholinesterase inhibitors 5.4 Curare 5.5 Synthesis inhibitors 5.6 Release inhibitors 6 Comparative biology and evolution 7 History 8 References 9 Bibliography 10 External links Chemistry Acetylcholine is a choline molecule that has been acetylated at the oxygen atom. Because of the presence of a highly polar, charged ammonium group, acetylcholine does not penetrate lipid membranes. Because of this, when the drug is introduced externally, it remains in the extracellular space and does not pass through the blood -- brain barrier. A synonym of this drug is miochol. Biochemistry Acetylcholine is synthesized in certain neurons by the enzyme choline acetyltransferase from the compounds choline and acetyl - CoA. Cholinergic neurons are capable of producing ACh. An example of a central cholinergic area is the nucleus basalis of Meynert in the basal forebrain. The enzyme acetylcholinesterase converts acetylcholine into the inactive metabolites choline and acetate. This enzyme is abundant in the synaptic cleft, and its role in rapidly clearing free acetylcholine from the synapse is essential for proper muscle function. Certain neurotoxins work by inhibiting acetylcholinesterase, thus leading to excess acetylcholine at the neuromuscular junction, causing paralysis of the muscles needed for breathing and stopping the beating of the heart. Functions Acetylcholine pathway. Acetylcholine functions in both the central nervous system ( CNS ) and the peripheral nervous system ( PNS ). In the CNS, cholinergic projections from the basal forebrain to the cerebral cortex and hippocampus support the cognitive functions of those target areas. In the PNS, acetylcholine activates muscles and is a major neurotransmitter in the autonomic nervous system. Cellular effects Main article : Acetylcholine receptor Acetylcholine processing in a synapse. After release acetylcholine is broken down by the enzyme acetylcholinesterase. Like many other biologically active substances, acetylcholine exerts its effects by binding to and activating receptors located on the surface of cells. There are two main classes of acetylcholine receptor, nicotinic and muscarinic. They are named for chemicals that can selectively activate each type of receptor without activating the other : muscarine is a compound found in the mushroom Amanita muscaria ; nicotine is found in tobacco. Nicotinic acetylcholine receptors are ligand - gated ion channels permeable to sodium, potassium, and calcium ions. In other words, they are ion channels embedded in cell membranes, capable of switching from a closed to open state when acetylcholine binds to them ; in the open state they allow ions to pass through. Nicotinic receptors come in two main types, known as muscle - type and neuronal - type. The muscle - type can be selectively blocked by curare, the neuronal - type by hexamethonium. The main location of muscle - type receptors is on muscle cells, as described in more detail below. Neuronal - type receptors are located in autonomic ganglia ( both sympathetic and parasympathetic ), and in the central nervous system. Muscarinic acetylcholine receptors have a more complex mechanism, and affect target cells over a longer time frame. In mammals, five subtypes of muscarinic receptors have been identified, labeled M1 through M5. All of them function as G protein - coupled receptors, meaning that they exert their effects via a second messenger system. The M1, M3, and M5 subtypes are G - coupled ; they increase intracellular levels of IP and calcium by activating phospholipase C. Their effect on target cells is usually excitatory. The M2 and M4 subtypes are G / G - coupled ; they decrease intracellular levels of cAMP by inhibiting adenylate cyclase. Their effect on target cells is usually inhibitory. Muscarinic acetylcholine receptors are found in both the central nervous system and the peripheral nervous system of the heart, lungs, upper gastrointestinal tract, and sweat glands. Neuromuscular junction Muscles contract when they receive signals from motor neurons. The neuromuscular junction is the site of the signal exchange. The steps of this process in vertebrates occur as follows : ( 1 ) The action potential reaches the axon terminal. ( 2 ) Calcium ions flow into the axon terminal. ( 3 ) Acetylcholine is released into the synaptic cleft. ( 4 ) Acetylcholine binds to postsynaptic receptors. ( 5 ) This binding causes ion channels to open and allows sodium ions to flow into the muscle cell. ( 6 ) The flow of sodium ions across the membrane into the muscle cell generates an action potential which induces muscle contraction. Labels : A : Motor neuron axon B : Axon terminal C : Synaptic cleft D: Muscle cell E : Part of a Myofibril Main article : Neuromuscular junction Acetylcholine is the substance the nervous system uses to activate skeletal muscles, a kind of striated muscle. These are the muscles used for all types of voluntary movement, in contrast to smooth muscle tissue, which is involved in a range of involuntary activities such as movement of food through the gastrointestinal tract and constriction of blood vessels. Skeletal muscles are directly controlled by motor neurons located in the spinal cord or, in a few cases, the brainstem. These motor neurons send their axons through motor nerves, from which they emerge to connect to muscle fibers at a special type of synapse called the neuromuscular junction. When a motor neuron generates an action potential, it travels rapidly along the nerve until it reaches the neuromuscular junction, where it initiates an electrochemical process that causes acetylcholine to be released into the space between the presynaptic terminal and the muscle fiber. The acetylcholine molecules then bind to nicotinic ion - channel receptors on the muscle cell membrane, causing the ion channels to open. Calcium ions then flow into the muscle cell, initiating a sequence of steps that finally produce muscle contraction. Autonomic nervous system Components and connections of the parasympathetic nervous system. The autonomic nervous system controls a wide range of involuntary and unconscious body functions. Its main branches are the sympathetic nervous system and parasympathetic nervous system. Broadly speaking, the function of the sympathetic nervous system is to mobilize the body for action : the slogan often used for it is fight - or - flight. The function of the parasympathetic nervous system is to put the body in a state conducive to rest, regeneration, digestion, and reproduction : it is sometimes described using the slogans `` rest and digest '' or `` feed and breed ''. Both branches use acetylcholine, but in different ways. At a schematic level, the sympathetic and parasympathetic nervous systems are both organized in essentially the same way : preganglionic neurons in the central nervous system send projections to neurons located in autonomic ganglia ; these neurons then send output projections to virtually every tissue of the body. In both branches the internal connections -- the projections from the central nervous system to the autonomic ganglia -- use acetylcholine as neurotransmitter, and the receptors it activates are of the nicotinic type. In the parasympathetic nervous system the output connections -- the projections from ganglion neurons to tissues that do n't belong to the nervous system -- also release acetylcholine, acting on muscarinic receptors. In the sympathetic nervous system the output connections mainly release noradrenaline, although acetylcholine is released at a few points, such as the sudomotor innervation of the sweat glands. Direct vascular effects Acetylcholine in the serum exerts a direct effect on vascular tone by binding to muscarinic receptors present on vascular endothelium. These cells respond by increasing production of nitric oxide, which signals the surrounding smooth muscle to relax, leading to vasodilation. Central nervous system Micrograph of the nucleus basalis ( of Meynert ), which produces acetylcholine in the CNS. LFB - HE stain. In the central nervous system, ACh has a variety of effects on plasticity, arousal and reward. ACh has an important role in the enhancement of alertness when we wake up, in sustaining attention and in learning and memory. Damage to the cholinergic ( acetylcholine - producing ) system in the brain has been shown to be associated with the memory deficits associated with Alzheimer 's disease. ACh has also been shown to promote REM sleep. In the brainstem acetylcholine originates from the Pedunculopontine nucleus and laterodorsal tegmental nucleus collectively known as the meso pontine tegmentum area or pontomesencephalotegmental complex. In the basal forebrain, it originates from the basal nucleus of Meynert and medial septal nucleus : The pontomesencephalotegmental complex acts mainly on M1 receptors in the brainstem, deep cerebellar nuclei, pontine nuclei, locus coeruleus, raphe nucleus, lateral reticular nucleus and inferior olive. It also projects to the thalamus, tectum, basal ganglia and basal forebrain. Basal nucleus of Meynert acts mainly on M1 receptors in the neocortex. Medial septal nucleus acts mainly on M1 receptors in the hippocampus and parts of the cerebral cortex. In addition, ACh acts as an important internal transmitter in the striatum, which is part of the basal ganglia. It is released by cholinergic interneurons. In humans, non-human primates and rodents, these interneurons respond to salient environmental stimuli with responses that are temporally aligned with the responses of dopaminergic neurons of the substantia nigra. Memory Acetylcholine has been implicated in learning and memory in several ways. The anticholinergic drug, scopolamine, impairs acquisition of new information in humans and animals. In animals, disruption of the supply of acetylcholine to the neocortex impairs the learning of simple discrimination tasks, comparable to the acquisition of factual information and disruption of the supply of acetylcholine to the hippocampus and adjacent cortical areas produces forgetting comparable to anterograde amnesia in humans. Diseases and disorders Myasthenia gravis The disease myasthenia gravis, characterized by muscle weakness and fatigue, occurs when the body inappropriately produces antibodies against acetylcholine nicotinic receptors, and thus inhibits proper acetylcholine signal transmission. Over time, the motor end plate is destroyed. Drugs that competitively inhibit acetylcholinesterase ( e.g., neostigmine, physostigmine, or primarily pyridostigmine ) are effective in treating this disorder. They allow endogenously released acetylcholine more time to interact with its respective receptor before being inactivated by acetylcholinesterase in the synaptic cleft ( the space between nerve and muscle ). Pharmacology Blocking, hindering or mimicking the action of acetylcholine has many uses in medicine. Drugs acting on the acetylcholine system are either agonists to the receptors, stimulating the system, or antagonists, inhibiting it. Acetylcholine receptor agonists and antagonists can either have an effect directly on the receptors or exert their effects indirectly, e.g., by affecting the enzyme acetylcholinesterase, which degrades the receptor ligand. Agonists increase the level of receptor activation, antagonists reduce it. Acetylcholine itself does not have therapeutic value as a drug for intravenous administration because of its multi-faceted action ( non-selective ) and rapid inactivation by cholinesterase. However, it is used in the form of eye drops to cause constriction of the pupil during cataract surgery, which facilitates quick post-operational recovery. Nicotine Nicotine binds to and activates nicotinic acetylcholine receptors, mimicking the effect of acetylcholine at these receptors. When ACh interacts with a nicotinic ACh receptor, it opens a Na+ channel and Na+ ions flow into the membrane. This causes a depolarization, and results in an excitatory post-synaptic potential. Thus, ACh is excitatory on skeletal muscle ; the electrical response is fast and short - lived. Atropine Atropine is a non-selective competitive antagonist with Acetylcholine at muscarinic receptors. Cholinesterase inhibitors Main article : Cholinesterase inhibitors Many ACh receptor agonists work indirectly by inhibiting the enzyme acetylcholinesterase. The resulting accumulation of acetylcholine causes continuous stimulation of the muscles, glands, and central nervous system, which can result in fatal convulsions if the dose is high. They are examples of enzyme inhibitors, and increase the action of acetylcholine by delaying its degradation ; some have been used as nerve agents ( Sarin and VX nerve gas ) or pesticides ( organophosphates and the carbamates ). Many toxins and venoms produced by plants and animals also contain cholinesterase inhibitors. In clinical use, they are administered in low doses to reverse the action of muscle relaxants, to treat myasthenia gravis, and to treat symptoms of Alzheimer 's disease ( rivastigmine, which increases cholinergic activity in the brain ). Curare Main article : Curare Synthesis inhibitors Organic mercurial compounds, such as methylmercury, have a high affinity for sulfhydryl groups, which causes dysfunction of the enzyme choline acetyltransferase. This inhibition may lead to acetylcholine deficiency, and can have consequences on motor function. Release inhibitors Botulinum toxin ( Botox ) acts by suppressing the release of acetylcholine, whereas the venom from a black widow spider ( alpha - latrotoxin ) has the reverse effect. ACh inhibition causes paralysis. When bitten by a black widow spider, one experiences the wastage of ACh supplies and the muscles begin to contract. If and when the supply is depleted, paralysis occurs. Comparative biology and evolution Acetylcholine is used by animals in all domains of life for a variety of purposes. It is believed that choline, a precursor to acetylcholine, was used by single celled organisms billions of years ago for synthesizing cell membrane phospholipids. Following the evolution of choline transporters, the abundance of intracellular choline paved the way for choline to become incorporated into other synthetic pathways, including acetylcholine production. Acetylcholine is now used by bacteria, fungi, and a variety of other animals. Interestingly, many of the uses of acetylcholine rely on its action on ion channels. The two major types of acetylcholine receptors, muscarinic and nicotinic receptors, have convergently evolved to be responsive to acetylcholine. This means that rather than having evolved from a common homolog, these receptors evolved from separate receptor families. It is estimated that the nicotinic receptor family dates back longer than 2.5 billion years. Likewise, muscarinic receptors are thought to have diverged from other GPCRs at least 0.5 billion years ago. Both of these receptor groups have evolved numerous subtypes with unique ligand affinities and signaling mechanisms. The diversity of the receptor types enables acetylcholine to creating varying responses depending on which receptor types are activated, and allow for acetylcholine to dynamically regulate physiological processes. History Acetylcholine ( ACh ) was first identified in 1915 by Henry Hallett Dale for its actions on heart tissue. It was confirmed as a neurotransmitter by Otto Loewi, who initially gave it the name Vagusstoff because it was released from the vagus nerve. Both received the 1936 Nobel Prize in Physiology or Medicine for their work. Acetylcholine was also the first neurotransmitter to be identified. 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PMID 15944135. as PDF External links Warning over combining common medicines for elderly Neurotransmitters Amino acid - derived Major excitatory / inhibitory systems : Glutamate system : Agmatine Aspartic acid ( aspartate ) Cycloserine Glutamic acid ( glutamate ) Glutathione Glycine GSNO GSSG Kynurenic acid NAA NAAG Proline Serine ; GABA system : GABA GABOB GHB ; Glycine system : α - Alanine β - Alanine Glycine Hypotaurine Proline Sarcosine Serine Taurine ; GHB system : GHB T - HCA ( GHC ) Biogenic amines : Monoamines : 6 - OHM Dopamine Epinephrine ( adrenaline ) NAS ( normelatonin ) Norepinephrine ( noradrenaline ) Serotonin ( 5 - HT ) ; Trace amines : 3 - Iodothyronamine N - Methylphenethylamine N - Methyltryptamine m - Octopamine p - Octopamine Phenylethanolamine Phenethylamine Synephrine Tryptamine m - Tyramine p - Tyramine ; Others : Histamine Neuropeptides : See here instead. Lipid - derived Endocannabinoids : 2 - AG 2 - AGE ( noladin ether ) 2 - ALPI 2 - OG AA - 5 - HT Anandamide ( AEA ) DEA LPI NADA NAGly OEA Oleamide PEA RVD - Hpα SEA Virodhamine ( O - AEA ) Neurosteroids : See here instead. Nucleobase - derived Nucleosides : Adenosine system : Adenosine ADP AMP ATP Vitamin - derived Cholinergic system : Acetylcholine Miscellaneous Gasotransmitters : Carbon monoxide ( CO ) Hydrogen sulfide ( H S ) Nitric oxide ( NO ) ; Candidates : Acetaldehyde Ammonia ( NH ) Carbonyl sulfide ( COS ) Nitrous oxide ( N O ) Sulfur dioxide ( SO ) Acetylcholine receptor modulators Muscarinic acetylcholine receptor modulators mAChRs Agonists 77 - LH - 28 - 1 AC - 42 AC - 260,584 Aceclidine Acetylcholine AF30 AF150 ( S ) AF267B Alvameline AQRA - 741 Arecoline Bethanechol Bevonium Butyrylcholine Carbachol CDD - 0034 CDD - 0078 CDD - 0097 CDD - 0098 CDD - 0102 Cevimeline Choline cis - Dioxolane Clozapine Desmethylclozapine ( norclozapine ) Ethoxysebacylcholine Itameline LY - 593,039 L - 689,660 LY - 2,033,298 McNA343 Methacholine Milameline Muscarine NGX - 267 Ocvimeline Oxotremorine PD - 151,832 Pilocarpine RS86 Sabcomeline SDZ 210 - 086 Sebacylcholine Suberyldicholine Talsaclidine Tazomeline Thiopilocarpine Vedaclidine VU - 0029767 VU - 0090157 VU - 0152099 VU - 0152100 VU - 0238429 WAY - 132,983 Xanomeline YM - 796 Antagonists 3 - Quinuclidinyl benzilate 4 - DAMP Aclidinium bromide ( + formoterol ) Abediterol AF - DX 250 AF - DX 384 Ambutonium bromide Anisodamine Anisodine Antihistamines ( first - generation ) ( e.g., brompheniramine, buclizine, captodiame, chlorphenamine ( chlorpheniramine ), cinnarizine, clemastine, cyproheptadine, dimenhydrinate, dimetindene, diphenhydramine, doxylamine, meclizine, mepyramine ( pyrilamine ), mequitazine, perlapine, phenindamine, pheniramine, phenyltoloxamine, promethazine, propiomazine, triprolidine ) AQ - RA 741 Atropine Atropine methonitrate Atypical antipsychotics ( e.g., clozapine, fluperlapine, olanzapine ( + fluoxetine ), rilapine, quetiapine, tenilapine, zotepine ) Benactyzine Benzatropine ( benztropine ) Benzilone Benzilylcholine mustard Benzydamine BIBN 99 Biperiden Bornaprine Camylofin CAR - 226,086 CAR - 301,060 CAR - 302,196 CAR - 302,282 CAR - 302,368 CAR - 302,537 CAR - 302,668 Caramiphen Cimetropium bromide Clidinium bromide Cloperastine CS - 27349 Cyclobenzaprine Cyclopentolate Darifenacin DAU - 5884 Desfesoterodine Dexetimide DIBD Dicycloverine ( dicyclomine ) Dihexyverine Difemerine Diphemanil metilsulfate Ditran EA - 3167 EA - 3443 EA - 3580 EA - 3834 Emepronium bromide Etanautine Etybenzatropine ( ethybenztropine ) Fenpiverinium Fentonium Fesoterodine Flavoxate Glycopyrronium bromide ( + beclometasone / formoterol, + indacaterol ) Hexahydrodifenidol Hexahydrosiladifenidol Hexbutinol Hexocyclium Himbacine HL - 031,120 Homatropine Imidafenacin Ipratropium bromide ( + salbutamol ) Isopropamide J - 104,129 Hyoscyamine Mamba toxin 3 Mamba toxin 7 Mazaticol Mebeverine Meladrazine Mepenzolate Methantheline Methoctramine Methylatropine Methylhomatropine Methylscopolamine Metixene Muscarinic toxin 7 N - Ethyl - 3 - piperidyl benzilate N - Methyl - 3 - piperidyl benzilate Nefopam Octatropine methylbromide ( anisotropine methylbromide ) Orphenadrine Otenzepad ( AF - DX 116 ) Otilonium bromide Oxapium iodide Oxitropium bromide Oxybutynin Oxyphencyclimine Oxyphenonium bromide PBID PD - 102,807 PD - 0298029 Penthienate Pethidine pFHHSiD Phenglutarimide Phenyltoloxamine Pipenzolate bromide Piperidolate Pirenzepine Piroheptine Pizotifen Poldine Pridinol Prifinium bromide Procyclidine Profenamine ( ethopropazine ) Propantheline bromide Propiverine Quinidine Revefenacin Rociverine RU - 47,213 SCH - 57,790 SCH - 72,788 SCH - 217,443 Scopolamine ( hyoscine ) Scopolamine butylbromide ( hyoscine butylbromide ) Silahexacyclium Sofpironium bromide Solifenacin SSRIs ( e.g., femoxetine, paroxetine ) Telenzepine Terodiline Tetracyclic antidepressants ( e.g., amoxapine, maprotiline, mianserin, mirtazapine ) Tiemonium iodide Timepidium bromide Tiotropium bromide Tiquizium bromide Tofenacin Tolterodine Tricyclic antidepressants ( e.g., amitriptyline ( + perphenazine ), amitriptylinoxide, butriptyline, cidoxepin, clomipramine, desipramine, desmethyldesipramine, dibenzepin, dosulepin ( dothiepin ), doxepin, imipramine, lofepramine, nitroxazepine, northiaden ( desmethyldosulepin ), nortriptyline, protriptyline, quinupramine, trimipramine ) Tridihexethyl Trihexyphenidyl Trimebutine Tripitamine ( tripitramine ) Tropacine Tropatepine Tropicamide Trospium chloride Typical antipsychotics ( e.g., chlorpromazine, chlorprothixene, cyamemazine ( cyamepromazine ), loxapine, mesoridazine, thioridazine ) Umeclidinium bromide ( + vilanterol ) WIN - 2299 Xanomeline Zamifenacin Precursors ( and prodrugs ) Acetyl - coA Adafenoxate Choline ( lecithin ) Citicoline Cyprodenate Dimethylethanolamine Glycerophosphocholine Meclofenoxate ( centrophenoxine ) Phosphatidylcholine Phosphatidylethanolamine Phosphorylcholine Pirisudanol See also : Receptor / signaling modulators Nicotinic acetylcholine receptor modulators Acetylcholine metabolism / transport modulators Nicotinic acetylcholine receptor modulators nAChRs Agonists ( and PAMs ) 5 - HIAA A-84,543 A-366,833 A-582,941 A-867,744 ABT - 202 ABT - 418 ABT - 560 ABT - 894 Acetylcholine Altinicline Anabasine Anatoxin - a AR - R17779 Bephenium hydroxynaphthoate Butinoline Butyrylcholine Carbachol Choline Cotinine Cytisine Decamethonium Desformylflustrabromine Dianicline Dimethylphenylpiperazinium Epibatidine Epiboxidine Ethanol ( alcohol ) Ethoxysebacylcholine EVP - 4473 EVP - 6124 Galantamine GTS - 21 Ispronicline Ivermectin JNJ - 39393406 Levamisole Lobeline MEM - 63,908 ( RG - 3487 ) Morantel Nicotine ( tobacco ) NS - 1738 PHA - 543,613 PHA - 709,829 PNU - 120,596 PNU - 282,987 Pozanicline Pyrantel Rivanicline RJR - 2429 Sazetidine A SB - 206553 Sebacylcholine SIB - 1508Y SIB - 1553A SSR - 180,711 Suberyldicholine Suxamethonium ( succinylcholine ) Suxethonium ( succinyldicholine ) TC - 1698 TC - 1734 TC - 1827 TC - 2216 TC - 5214 TC - 5619 TC - 6683 Tebanicline Tribendimidine Tropisetron UB - 165 Varenicline WAY - 317,538 XY - 4083 Antagonists ( and NAMs ) 18 - MAC 18 - MC α - Neurotoxins ( e.g., α - bungarotoxin, α - cobratoxin, α - conotoxin, many others ) ABT - 126 Alcuronium Allopregnanolone Amantadine Anatruxonium AQW051 Atracurium Barbiturates ( e.g., pentobarbital, sodium thiopental ) BNC - 210 Bungarotoxins ( e.g., α - bungarotoxin, κ - bungarotoxin ) Bupropion BW - A444 Candocuronium iodide ( chandonium iodide ) Chlorisondamine Cisatracurium Coclaurine Coronaridine Curare Cyclopropane Dacuronium bromide Decamethonium Dehydronorketamine Desflurane Dextromethorphan Dextropropoxyphene Dextrorphan Diadonium DHβE Dihydrochandonium Dimethyltubocurarine ( metocurine ) Dioscorine Dipyrandium Dizocilpine ( MK - 801 ) Doxacurium Encenicline Enflurane Erythravine Esketamine Fazadinium Gallamine Gantacurium chloride Halothane Hexafluronium Hexamethonium ( benzohexonium ) Hydroxybupropion Hydroxynorketamine Ibogaine Isoflurane Ketamine Kynurenic acid Laudanosine Laudexium ( laudolissin ) Levacetylmethadol Levomethadone Malouetine ME - 18 - MC Mecamylamine Memantine Methadone Methorphan ( racemethorphan ) Methyllycaconitine Metocurine Mivacurium Morphanol ( racemorphan ) Neramexane Nitrous oxide Norketamine Pancuronium bromide Pempidine Pentamine Pentolinium Phencyclidine Pipecuronium bromide Progesterone Promegestone Radafaxine Rapacuronium bromide Reboxetine Rocuronium bromide Sevoflurane Stercuronium iodide Surugatoxin Thiocolchicoside Toxiferine Tramadol Trimetaphan camsilate ( trimethaphan camsylate ) Tropeinium Tubocurarine Vanoxerine Vecuronium bromide Xenon Precursors ( and prodrugs ) Acetyl - coA Adafenoxate Choline ( lecithin ) Citicoline Cyprodenate Dimethylethanolamine Glycerophosphocholine Meclofenoxate ( centrophenoxine ) Phosphatidylcholine Phosphatidylethanolamine Phosphorylcholine Pirisudanol See also : Receptor / signaling modulators Muscarinic acetylcholine receptor modulators Acetylcholine metabolism / transport modulators Acetylcholine metabolism and transport modulators Enzyme ( modulators ) ChAT Inhibitors : 1 - ( - Benzoylethyl ) pyridinium 2 - ( α - Naphthoyl ) ethyltrimethylammonium 3 - Chloro - 4 - stillbazole 4 - ( 1 - Naphthylvinyl ) pyridine Acetylseco hemicholinium - 3 Acryloylcholine AF64A B115 BETA CM - 54,903 N, N - Dimethylaminoethylacrylate N, N - Dimethylaminoethylchloroacetate AChE Inhibitors : Reversible : Carbamates : Aldicarb Aminocarb Bendiocarb Bufencarb Carbaryl Carbendazim Carbetamide Carbofuran Carbosulfan Chlorbufam Chloropropham Dimetilan Ethienocarb Ethiofencarb Fenobucarb Formetanate Formparanate Methiocarb Methomyl Metolcarb Miotine Oxamyl Phenmedipham Pinmicarb Pirimicarb Propamocarb Propham Propoxur Thiofanox ; Stigmines : Distigmine Eptastigmine Ganstigmine Neostigmine Phenserine Physostigmine Pyridostigmine Quilostigmine Rivastigmine Terestigmine ; Others : Acotiamide Ambenonium Caffeine Donepezil EA - 3990 EA - 4056 Edrophonium Galantamine Huperzine A Ipidacrine Itopride Ladostigil Minaprine T - 1123 Tacrine Zanapezil Irreversible : Organophosphates : Acephate Anatoxin - a ( S ) Azinphos - ethyl Azinphos - methyl BAY - 29952 Bensulide Cadusafos Carbophenothion Chlorethoxyfos Chlorfenvinphos Chlorpyrifos Chlorpyrifos - methyl Coumaphos Cyanophos Cyclosarin Demephion Demeton Demeton - S - methyl Dialifor Diazinon Dichlorvos Dicrotophos Diisopropyl fluorophosphate Diisopropylphosphate Dimefox Dimethoate Dimethyl 4 - ( methylthio ) phenyl phosphate Dioxathion Disulfoton EA - 3148 Echothiophate Endothion Ethion Ethoprop Fenamiphos Fenitrothion Fenthion Fonofos Formothion Fosthiazate GV Hexaethyl tetraphosphate Isofluorophate Isoxathion Leptophos Malaoxon Malathion Methamidophos Methidathion Methyl phenkapton Metrifonate Mevinphos Monocrotophos Naled Novichok agent Omethoate Oxydemeton - methyl Paraoxon Parathion Parathion - methyl Phorate Phosalone Phosfolan Phosmet Phosphamidon Phoxim Pirimiphos - methyl Profenofos Prothoate Sarin Soman Tabun Tebupirimfos Temefos Terbufos Tetrachlorvinphos Triazofos Tribufos Trichlorfon Trichloronate Tricresyl phosphate VE VG VM VR VX ; Others : Demecarium Fasciculins ( green mamba toxins ) ( 1, 2, 3, 4 ) Onchidal ( Onchidella binneyi ) Unsorted : α - Pinene α - Viniferin Affinine Affinisine Arisugacin A Bulbocapnine Conodurine Coronaridine Corydaline Corynoline Crimidine Cyclanoline Cymserine Harmaline Kobophenol A Lactucopicrin Lycorine Phosacetim Rosmarinic acid Stercuronium iodide Taspine Tetrahydrocannabinol Ungeremine Ungiminorine Reactivators : Asoxime chloride Methoxime Obidoxime Pralidoxime Trimedoxime bromide BChE Inhibitors : Affinine Affinisine Conodurine Cymserine Ladostigil Profenamine ( ethopropazine ) Rivastigmine Tacrine ZINC - 12613047 Many of the other AChE inhibitors listed above Transporter ( modulators ) CHT Inhibitors : Hemicholinium - 3 ( hemicholine ) Triethylcholine Enhancers : Coluracetam VAChT Inhibitors : Vesamicol Release ( modulators ) Inhibitors SNAP - 25 inactivators : Botulinum toxin ( A, C, E ) VAMP inactivators : Botulinum toxin ( B, D, F, G ) Others : Bungarotoxins ( β - bungarotoxin, γ - bungarotoxin ) Enhancers LPHN agonists : α - Latrotoxin Others : Atracotoxin ( e.g., robustoxin, versutoxin ) Crotoxin See also : Receptor / signaling modulators Muscarinic acetylcholine receptor modulators Nicotinic acetylcholine receptor modulators LCCN : sh85000467 GND : 4141256 - 4 Biology portal Neuroscience portal Retrieved from `` https://en.wikipedia.org/w/index.php?title=Acetylcholine&oldid=831518669 '' Categories : Acetate esters Acetylcholine Choline esters Cholinergics Muscarinic agonists Nicotinic agonists Quaternary ammonium compounds Hidden categories : E number from Wikidata ECHA InfoCard ID from Wikidata Articles without EBI source Articles without InChI source Articles without UNII source Drugs missing an ATC code Drugs with no legal status Articles containing unverified chemical infoboxes Drugs that are a physiological drug Wikipedia articles with LCCN identifiers Wikipedia articles with GND identifiers Talk Contents About Wikipedia Wikiquote Afrikaans Български Bosanski Català Cebuano Čeština Dansk Deutsch Eesti Ελληνικά Español Esperanto Euskara فارسی Français Gaeilge Galego 한국어 Հայերեն Hrvatski Bahasa Indonesia Íslenska Italiano עברית ქართული Қазақша Latina Lietuvių Magyar Македонски മലയാളം Bahasa Melayu Nederlands 日本 語 Norsk Norsk nynorsk Occitan Oʻzbekcha / ўзбекча Polski Português Română Русский Scots සිංහල Simple English Slovenčina Slovenščina Српски / srpski Srpskohrvatski / српскохрватски Suomi Svenska Tagalog Тоҷикӣ Türkçe Українська اردو Tiếng Việt 中文 50 more Edit links This page was last edited on 21 March 2018, at 00 : 20. 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Question: where is acetylcholine released from to stimulate muscle contraction
Answer: the neuromuscular junction