Editing Acetylcholine (section)

==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.

===Nicotinic receptors===
{{main|Nicotinic receptor}}
Nicotine binds to and activates [[nicotinic acetylcholine receptor]]s, mimicking the effect of acetylcholine at these receptors. ACh opens a '''Na<sup>+</sup>''' '''channel''' upon binding so that Na<sup>+</sup> flows into the cell. 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. [[Curare]]s are arrow poisons, which act at nicotinic receptors and have been used to develop clinically useful therapies.

===Muscarinic receptors===
{{main|Muscarinic receptor}}
Muscarinic receptors form '''[[G protein-coupled receptor]]''' complexes in the [[cell membrane]]s of [[neuron]]s and other cells. [[Atropine]] is a non-selective competitive antagonist with Acetylcholine at muscarinic receptors.

===Cholinesterase inhibitors===
{{Main|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 agent]]s ([[Sarin]] and [[VX (nerve agent)|VX]] nerve gas) or [[pesticide]]s ([[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{{why?|date=July 2023}} to reverse the action of [[muscle relaxant]]s, to treat [[myasthenia gravis]], and to treat symptoms of [[Alzheimer's disease]] ([[rivastigmine]], which increases cholinergic activity in the brain).

===Synthesis inhibitors===
Organic [[Mercury (element)|mercurial]] compounds, such as [[methylmercury]], have a high affinity for [[thiol|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 [[latrodectus|black widow spider]] ([[alpha-latrotoxin]]) has the reverse effect. ACh inhibition causes [[paralysis]]. When bitten by a [[latrodectus|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.