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Acetylcholine
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== Function == Acetylcholine is used 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]]. It plays an important role in regulating the [[inflammation|inflammatory]] response and is used at the neuromuscular junction by motor neurons in order to activate muscles. In the [[central nervous system]], acetylcholine modulates arousal and [[temperature]] regulation, is important for attention, memory and motivation, and may play a role in [[central fatigue]]. === General Function Summary === As a neurotransmitter, acetylcholine is produced in nerve cells. Any cell that produces or is affected by acetylcholine is called cholinergic. In the nervous system, acetylcholine typically travels from the axon to the dendrite of the next nerve cell across the synaptic cleft. In muscle cells, it travels to the receptors on the muscle fiber, called the motor end plate. Acetylcholine can activate receptors, such as the [[nicotonic]] receptors or [[Muscarinic acetylcholine receptor|muscarinic]] receptors. These receptors can also be activated by, or blocked by, other molecules such as nicotine and muscarine. Muscarinic receptors are typically found in the parasypathetic nervous system, whereas nicotonic receptors are found in the [[central nervous system]], [[peripheral nervous system]], and [[Neuromuscular junction|neuromuscular]] junctions. Nicotonic receptors are classified as ligand-gated [[Ion channel|ion channels]] - when activated they open and allow ions like K+, Na+, and Ca+ to move in or out of the cell. Muscarinic receptors exert their effects on cells via a secondary messenger system. Closing of the gate is completed by [[Acetylcholinesterase]] ( AChE) which catalyzes the breakdown of acetylcholine into [[choline]] and acetic acid, which allows the ion gate to close. Each molecule of AChE can degrade about 25,000 molecules of acetylcholine (ACh) per second. If the AChE molecule is blocked, breakdown of ACh will not be completed and the gate will remain open. If the AChE is blocked on a muscle fiber, the fiber will remain contracted.<ref>{{Cite book | title = Concepts of Biology – 1st Canadian Edition| pages=Chapter 19.4|isbn=|edition=1 | volume = 1|language=English| title-link = |url=ttps://opentextbc.ca/biology/chapter/19-4-muscle-contraction-and-locomotion/ | access-date = 2020-05-28 | date = June 13, 2019| publisher = B.C. Open Textbook Collection | last = Molnar | first = Charles | author-link = | last2 = Gair | first2 = Jane | author-link2 = |veditors=|others=|doi=|oclc=|quote=|archive-url=|archive-date=|location=|editor-last = |editor-first = | editor1-link = |editor-last2 = |editor-first2 = }}</ref> Various duration and strength AChE blockers exist. Short-duration or reversible AChE blockers have been developed as medications, as short-term blocking of AChE can allow the ion gates to stay open longer and increase ACh availability. Long-duration and irreversible AChE blockers, including Nerve Gas, can cause various symptoms up to and including paralysis and death. <ref>{{Cite journal | last = Čolović| first = Mirjana B | last2 = Krstić| first2 = Danijela Z | last3 = Lazarević-Pašti | first3 = Tamara D | last4 = Bondžić| first4 = Aleksandra M | last5 = Vasić| first5 = Vesna M | date = May 2013 | title = Acetylcholinesterase Inhibitors: Pharmacology and Toxicology | url = https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3648782/ | journal = Current Neuropharmacology | volume = 11 | issue = 3 | pages = 315–335|doi=10.2174/1570159X11311030006|issn=1570-159X|pmc=3648782|pmid=24179466|quote=|access-date=|via=}}</ref>
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