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Acetylcholine
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'''Acetylcholine''' is a [[neurotransmitter]] that is thought to play a role in many human diseases including [[Myalgic encephalomyelitis|myalgic encephalomyelitis]] and [[Postural orthostatic tachycardia syndrome|postural orthostatic tachychardia syndrome]]. == 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> ==Immune system== The [[vagus nerve]] speaks directly to the [[immune system]] via acetylcholine.<ref>{{Cite news |url =https://www.sciencedaily.com/releases/2007/10/071024083630.htm | title = Direct Route From The Brain To The Immune System Discovered|work=ScienceDaily | access-date = 2018-08-10|language=en}}</ref><ref>{{Cite news |url =http://www3.imperial.ac.uk/newsandeventspggrp/imperialcollege/newssummary/news_24-2-2015-14-16-10 | title = Scientists uncover new role for neurotransmitter that helps fight infection {{!}} Imperial News {{!}} Imperial College London|work=Imperial News | access-date = 2018-08-10|language=en-GB}}</ref><ref>{{Cite journal | last = Darby | first = Matthew | last2 = Schnoeller | first2 = Corinna | last3 = Vira | first3 = Alykhan | last4 = Culley | first4 = Fiona | last5 = Bobat | first5 = Saeeda | last6 = Logan | first6 = Erin | last7 = Kirstein | first7 = Frank | last8 = Wess | first8 = Jürgen | last9 = Cunningham | first9 = Adam F. | date = 2015-01-28 | title = The M3 Muscarinic Receptor Is Required for Optimal Adaptive Immunity to Helminth and Bacterial Infection | url =http://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1004636 | journal = PLOS Pathogens|language=en | volume = 11 | issue = 1| pages = e1004636|doi=10.1371/journal.ppat.1004636|issn=1553-7374|pmid=25629518}}</ref> Acetylcholine plays a role in [[innate immune system|innate immunity]] through nicotinic [[acetylcholine receptors]] and in the [[adaptive immune system|adaptive immune response]] via M3 muscarinic acetylcholine receptors (M3R).<ref>{{Cite journal | last = Darby | first = Matthew | last2 = Schnoeller | first2 = Corinna | last3 = Vira | first3 = Alykhan | last4 = Culley | first4 = Fiona | last5 = Bobat | first5 = Saeeda | last6 = Logan | first6 = Erin | last7 = Kirstein | first7 = Frank | last8 = Wess | first8 = Jürgen | last9 = Cunningham | first9 = Adam F. | date = 2015-01-28 | title = The M3 Muscarinic Receptor Is Required for Optimal Adaptive Immunity to Helminth and Bacterial Infection | url =http://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1004636 | journal = PLOS Pathogens|language=en | volume = 11 | issue = 1| pages = e1004636|doi=10.1371/journal.ppat.1004636|issn=1553-7374|pmid=25629518}}</ref> ===Muscarinic receptors=== Knockout mice, that is mice lacking the gene that encodes for M3R, had impaired response to bacterial infection, while normal mice given a muscarinic [[agonist]] (to increase the activity of M3R) had enhanced production of [[Interleukin 13|IL-13]] and [[IFN-γ]].<ref>{{Cite journal | last = Darby | first = Matthew | last2 = Schnoeller | first2 = Corinna | last3 = Vira | first3 = Alykhan | last4 = Culley | first4 = Fiona | last5 = Bobat | first5 = Saeeda | last6 = Logan | first6 = Erin | last7 = Kirstein | first7 = Frank | last8 = Wess | first8 = Jürgen | last9 = Cunningham | first9 = Adam F. | date = 2015-01-28 | title = The M3 Muscarinic Receptor Is Required for Optimal Adaptive Immunity to Helminth and Bacterial Infection | url =http://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1004636 | journal = PLOS Pathogens|language=en | volume = 11 | issue = 1| pages = e1004636|doi=10.1371/journal.ppat.1004636|issn=1553-7374|pmid=25629518}}</ref> Another study used a muscarinic agonist and an [[antagonist]] (reduce activity) and found antagonist suppressed the immune response while the agonist exaggerated it.<ref>{{Cite journal | last = Razani-Boroujerdi | first = Seddigheh | last2 = Behl | first2 = Muskaan | last3 = Hahn | first3 = Fletcher F. | last4 = Pena-Philippides | first4 = Juan Carlos | last5 = Hutt | first5 = Julie | last6 = Sopori | first6 = Mohan L. | date = Feb 2008 | title = Role of muscarinic receptors in the regulation of immune and inflammatory responses |url =https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2323336/ | journal = Journal of neuroimmunology | volume = 194 | issue = 1-2 | pages = 83–88|doi=10.1016/j.jneuroim.2007.11.019|issn=0165-5728|pmid=18190972}}</ref> ===Mast cells=== Several studies suggest a relationship between [[autonomic nervous system]] dysfunction and [[mast cell]] activation via acetylcholine. One study found that acetylcholine via muscarinic receptors strongly inhibited the release of [[histamine]] in [[mucosal]] mast cells.<ref>{{Cite journal | title = Acetylcholine via Muscarinic Receptors Inhibits Histamine Release from Human Isolated Bronchi | url = http://www.atsjournals.org/doi/full/10.1164/ajrccm.156.2.96-12079#.V7vo-ZMrLMV|journal =American Journal of Respiratory and Critical Care Medicine|volume =|issue = | pages =|language=en|doi=10.1164/ajrccm.156.2.96-12079#.v7vo-zmrlmv}}</ref> The activity of [[acetylcholinesterase]], an enzyme that breaks down acetylcholine, was found to be significantly increased in 64% of patients experiencing flares of [[ulcerative colitis]].<ref>https://www.myknowtions.com/portfolio/autonomic-nervous-alterations-and-mast-cell-degranulation-in-the-exacerbation-of-ulcerative-colitis</ref> ==In human disease== ===Myasthenia Gravis=== Autoantibodies to acetylcholine receptors alpha subunit have been found in patients with [[myasthenia gravis]]. These cross react with [[herpesvirus]] glycoprotein D. <ref>{{cite book | last1 = Angelini | first1 = Lucia | last2 = Bardare | first2 = Maria | last3 = Martini | first3 = Alberto| year = 2002 | title = Immune-mediated Disorders of the Central Nervous System in Children | url =https://books.google.com/books?id=5trQOK8hcZUC&pg=PA7&lpg=PA7&dq=coxsackie+b+acetylcholine&source=bl&ots=zhup8ZXq68&sig=CxDwQCHO8-OMBYkcp4EayjnDKnw&hl=en&sa=X&ved=0ahUKEwjflpmqg9fOAhWBeSYKHSR4Dh0Q6AEIMTAD#v=onepage&q=coxsackie%20b%20acetylcholine&f=false}}</ref> Antibodies to acetylcholine receptor and [[Herpes simplex virus#HSV-1|HSV-1]] antigens crossreact.<ref>{{Cite journal | last = Gebhardt | first = B.M. | date = 2000-06-26 | title = Evidence for antigenic cross-reactivity between herpesvirus and the acetylcholine receptor |url =http://www.ncbi.nlm.nih.gov/pubmed/10742556 | journal = Journal of Neuroimmunology | volume = 105 | issue = 2 | pages = 145–153|issn=0165-5728|pmid=10742556}}</ref> [[B cell]]s from myasthenia gravis patient stimulated ''in vitro'' by [[Epstein-Barr virus]] (EBV) produced acetylcholine autoantibodies.<ref>{{Cite journal | last = Brenner | first = T. | last2 = Timore | first2 = Y. | last3 = Wirguin | first3 = I. | last4 = Abramsky | first4 = O. | last5 = Steinitz | first5 = M. | date = Oct 1989 | title = In vitro synthesis of antibodies to acetylcholine receptor by Epstein-Barr virus-stimulated B-lymphocytes derived from patients with myasthenia gravis |url =http://www.ncbi.nlm.nih.gov/pubmed/2553772 | journal = Journal of Neuroimmunology | volume = 24 | issue = 3 | pages = 217–222|issn=0165-5728|pmid=2553772}}</ref> Ongoing EBV infection of the [[thymus]] has been posited as a causative agent for the production of aceytlcholine receptor autoantibodies in myasthenia gravis.<ref>{{Cite journal | last = Kaminski | first = Henry J. | last2 = Janos | first2 = Minarovits | title = Epstein-barr virus: Trigger for autoimmunity? | url = http://www.academia.edu/20258853/Epstein-barr_virus_Trigger_for_autoimmunity/ | journal = Annals of Neurology|language=en|issn=0364-5134}}</ref><ref>{{Cite web | url = http://journals.lww.com/neurologynow/_layouts/15/oaks.journals.mobile/post.aspx?blogId=2&postId=10 | title = Official Brain & Life Home Page | website = journals.lww.com|language=en | access-date = 2018-08-10}}</ref> ===Sjögren's syndrome=== Autoantibodies against muscarinic acetylcholine receptor on exocrine glands were found in patients with [[Sjögren's syndrome]].<ref>http://www.omicsonline.org/open-access/autoantibodies-against-muscarinic-acetylcholine-receptor-on-exocrine-glands-in-sjgren-syndrome-2161-1122.1000265.pdf</ref> ===Chronic fatigue syndrome=== Since at least the 1990s it has been theorized that CFS might be associated with abnormalities of acetylcholine neurotransmission. To test this hypothesis, a provocation study was performed using the acetylcholinesterase inhibitor [[pyridostigmine]]. The results did indicate that CFS patients' hypothalamuses are hypersensitive to cholinergic stimulation relative to matched healthy controls. <ref>{{Cite journal | last = Chaudhuri | first = A. | last2 = Majeed | first2 = T. | last3 = Dinan | first3 = T. | last4 = Behan | first4 = P.O. | date = Jan 1997 | title = Chronic Fatigue Syndrome: A Disorder of Central Cholinergic Transmission | url =http://www.tandfonline.com/doi/full/10.1300/J092v03n01_02 | journal = Journal of Chronic Fatigue Syndrome|language=en | volume = 3 | issue = 1 | pages = 3–16|doi=10.1300/J092v03n01_02|issn=1057-3321}}</ref> These results mirror similar, highly replicated findings showing that CFS patients' hypothalamuses are hypersensitive to serotonergic stimulation as well (see [[Buspirone challenge test]]). A 2003 study of 60 CFS patients found that 53.3% had detectable autoantibodies against the M1 muscarinic acetylcholine receptor. <ref>{{Cite journal | last = Tanaka | first = Susumu | last2 = Kuratsune | first2 = Hirohiko | last3 = Hidaka | first3 = Yoh | last4 = Hakariya | first4 = Yukiko | last5 = Tatsumi | first5 = Ke-Ita | last6 = Takano | first6 = Toru | last7 = Kanakura | first7 = Yuzuru | last8 = Amino | first8 = Nobuyuki | date = 2003-08-01 | title = Autoantibodies against muscarinic cholinergic receptor in chronic fatigue syndrome | url =http://www.spandidos-publications.com/10.3892/ijmm.12.2.225 | journal = International Journal of Molecular Medicine|doi=10.3892/ijmm.12.2.225|issn=1107-3756}}</ref> In 2015, a large German study found 29% of [[ME/CFS]] patients had elevated autoantibodies to M3 and M4 [[muscarinic acetylcholine receptor]]s, as well as ß2 [[adrenergic receptor]]s.<ref>{{Cite journal | last = Loebel | first = Madlen | last2 = Grabowski | first2 = Patricia | last3 = Heidecke | first3 = Harald | last4 = Bauer | first4 = Sandra | last5 = Hanitsch | first5 = Leif G. | last6 = Wittke | first6 = Kirsten | last7 = Meisel | first7 = Christian | last8 = Reinke | first8 = Petra | last9 = Volk | first9 = Hans-Dieter | date = Feb 2016 | title = Antibodies to β adrenergic and muscarinic cholinergic receptors in patients with Chronic Fatigue Syndrome | url =https://www.ncbi.nlm.nih.gov/pubmed/26399744 | journal = Brain, Behavior, and Immunity | volume = 52 | pages = 32–39|doi=10.1016/j.bbi.2015.09.013|issn=1090-2139|pmid=26399744}}</ref><ref>{{Cite web | url = http://www.meaction.net/2015/09/26/antibodies-found-in-subset-of-cfs-patients/ | title = Autoantibodies found in subset of CFS patients {{!}} #MEAction|website = [[The MEAction Network]]|language=en-US | access-date = 2018-08-10}}</ref> A 2016 Australian study found that ME/CFS patients had significantly greater numbers of [[single nucleotide polymorphism]]s associated with the gene encoding for M3 muscarinic acetylcholine receptors.<ref>{{Cite journal | last = Marshall-Gradisnik | first = Sonya | last2 = Smith | first2 = Peter | last3 = Nilius | first3 = Bernd | last4 = Staines | first4 = Donald R. | date = 2015-01-01 | title = Examination of Single Nucleotide Polymorphisms in Acetylcholine Receptors in Chronic Fatigue Syndrome Patients |url =https://doi.org/10.4137/III.S25105 | journal = Immunology and Immunogenetics Insights|language=en | volume = 7| pages=III.S25105|doi=10.4137/III.S25105|issn=1178-6345}}</ref> Several small clinical trials have been performed to assess the benefit of treatment with acetylcholinesterase inhibitors in CFS; one using pyridostigmine <ref>{{Cite journal | last = Kawamura | first = Yasuo | last2 = Kihara | first2 = Mikihiro | last3 = Nishimoto | first3 = Kazuhiro | last4 = Taki | first4 = Mayumi | date = May 2003 | title = Efficacy of a half dose of oral pyridostigmine in the treatment of chronic fatigue syndrome: three case reports |url =https://linkinghub.elsevier.com/retrieve/pii/S0928468003000075 | journal = Pathophysiology|language=en | volume = 9 | issue = 3 | pages = 189–194|doi=10.1016/S0928-4680(03)00007-5}}</ref> and another using galantamine. <ref>{{Cite journal | last = Snorrason | first = Ernir | last2 = Geirsson | first2 = Arni | last3 = Stefansson | first3 = Kari | date = Jan 1996 | title = Trial of a Selective Acetylcholinesterase Inhibitor, Galanthamine Hydrobromide, in the Treatment of Chronic Fatigue Syndrome | url =http://www.tandfonline.com/doi/full/10.1300/J092v02n02_04 | journal = Journal of Chronic Fatigue Syndrome|language=en | volume = 2 | issue = 2-3 | pages = 35–54|doi=10.1300/J092v02n02_04|issn=1057-3321}}</ref> Both trials showed improvement of symptoms on the treatment. The exact mechanism or mechanisms by which AChE inhibition might help in CFS are unclear due to how widely represented acetylcholine-responsive tissues are in the brain, (neuro)musculature, cranial and pre-ganglionic spinal autonomic nerves, vasculature, and peripheral C-fibers. Additionally, AChE inhibitors such as [[pyridostigmine]] are able to stimulate growth hormone secretion, and both CFS and POTS patients have been shown to have disturbed growth hormone levels. <ref>{{Cite journal | last = Berwaerts | first = J. | last2 = Moorkens | first2 = G. | last3 = Abs | first3 = R. | date = Apr 1998 | title = Secretion of growth hormone in patients with chronic fatigue syndrome | url =https://linkinghub.elsevier.com/retrieve/pii/S1096637498800361 | journal = Growth Hormone & IGF Research|language=en | volume = 8 | pages = 127–129|doi=10.1016/S1096-6374(98)80036-1}}</ref><ref>{{Cite journal | last = Moorkens | first = G. | last2 = Wynants | first2 = H. | last3 = Abs | first3 = R. | date = Apr 1998 | title = Effect of growth hormone treatment in patients with chronic fatigue syndrome: A preliminary study | url = https://linkinghub.elsevier.com/retrieve/pii/S1096637498800373 | journal = Growth Hormone & IGF Research|language=en | volume = 8 | pages = 131–133|doi=10.1016/S1096-6374(98)80037-3}}</ref><ref>{{Cite journal | last = Johansson | first = Madeleine | last2 = Ricci | first2 = Fabrizio | last3 = Schulte | first3 = Janin | last4 = Persson | first4 = Margaretha | last5 = Melander | first5 = Olle | last6 = Sutton | first6 = Richard | last7 = Hamrefors | first7 = Viktor | last8 = Fedorowski | first8 = Artur | date = 2021-04-21 | title = Circulating levels of growth hormone in postural orthostatic tachycardia syndrome | url =https://www.nature.com/articles/s41598-021-87983-5 | journal = Scientific Reports|language=en | volume = 11 | issue = 1 | pages = 8575|doi=10.1038/s41598-021-87983-5|issn=2045-2322}}</ref> Anecdotally, some ME/CFS patients have tried pyridostigmine (trade name [[Mestinon]]), with some success.<ref>{{Cite news |url =http://www.healthrising.org/blog/2016/06/17/mestinon-chronic-fatigue-vagus-nerve-stimulation-exercise/ | title = A Mestinon Miracle: Vagus Nerve Stimulating Drug Helps Long Time ME/CFS Patient Exercise - Health Rising | date = 2016-06-17|work=Health Rising | access-date = 2018-08-10|language=en-US}}</ref> A work in progress study of [[exercise intolerance]] in [[preload failure]] found that Mestinon improved exercise tolerance, but the study has not yet been published.<ref>{{Cite journal | last = Oliveira | first = R.K. | date = 2016 | title = Pyridostigmine for Exercise Intolerance Treatment in Preload Failure | url =https://www.atsjournals.org/doi/abs/10.1164/ajrccm-conference.2016.193.1_MeetingAbstracts.A5664 | journal = American Journal of Respiratory and Critical Care Medicine | volume = | pages=|via=}}</ref> ===Postural orthostatic tachycardia=== A small study of [[postural orthostatic tachycardia syndrome]] in children found that 24.39% of patients had acetylcholine receptor autoantibodies.<ref>{{Cite journal | last = Li | first = Jiawei | last2 = Zhang | first2 = Qingyou | last3 = Liao | first3 = Ying | last4 = Zhang | first4 = Chunyu | last5 = Hao | first5 = Hongjun | last6 = Du | first6 = Junbao | date = 2014-08-03 | title = The Value of Acetylcholine Receptor Antibody in Children with Postural Tachycardia Syndrome | url =https://link.springer.com/article/10.1007/s00246-014-0981-8 | journal = Pediatric Cardiology|language=en | volume = 36 | issue = 1 | pages = 165–170|doi=10.1007/s00246-014-0981-8|issn=0172-0643}}</ref> A small study of adult patients found elevated α1, β1 and β2 adrenergic receptor autoantibodies.<ref>{{Cite journal | last = Li | first = Hongliang | last2 = Yu | first2 = Xichun | last3 = Liles | first3 = Campbell | last4 = Khan | first4 = Muneer | last5 = Vanderlinde‐Wood | first5 = Megan | last6 = Galloway | first6 = Allison | last7 = Zillner | first7 = Caitlin | last8 = Benbrook | first8 = Alexandria | last9 = Reim | first9 = Sean | date = 2014-01-27 | title = Autoimmune Basis for Postural Tachycardia Syndrome | url =https://www.ahajournals.org/doi/abs/10.1161/JAHA.113.000755 | journal = Journal of the American Heart Association|language=EN | volume = 3 | issue = 1|doi=10.1161/jaha.113.000755|issn=2047-9980|pmc=3959717|pmid=24572257}}</ref> A small randomized crossover design trial found that patients with postural orthostatic tachychardia improved with Mestinon.<ref>{{Cite journal | last = Raj | first = S.R. | date = 2005-05-31 | title = Acetylcholinesterase Inhibition Improves Tachycardia in Postural Tachycardia Syndrome | url =https://www.ahajournals.org/doi/pdf/10.1161/circulationaha.104.497594 | journal = Circulation | volume = 111 | issue = 21 | pages = 2734–2740|doi=10.1161/circulationaha.104.497594|issn=0009-7322}}</ref> == Increasing and decreasing acetylcholine == Many classes of drugs including [[Benzodiazepine|benzodiazepines]], [[Opiod|opiods]], anesthetics, and some [[Antihistimane|antihistimanes]] such as [[Benadryl]] are anticholinergic.{{Citation needed}} During [[exercise]], levels of acetylcholine drop.<ref>Conlay, L. A., Sabournjian, L. A., and Wurtman, R. J. Exercise and neuromodulators: choline and acetylcholine in marathon runners.Int. J. Sports Med. 13(Suppl. 1):S141-142, 1992</ref> === Acetylcholinesterase inhibitors === [[Acetylcholinesterase]] is an enzyme that breaks down acetylcholine. Acetylcholinesterase inhibitors block or downregulate the activity of acetylcholinesterase; in turn, because there is less enzyme breaking down acetylcholine, the amount of circulating acetylcholine increases. The following compounds are acetylcholinesterase inhibitors: * [[pyridostigmine]] (Mestinon) - A peripheral AChE inhibitor, pyridostigmine is unable to cross the blood brain barrier due to its chemical structure. <ref>{{Cite journal | last = Anderson | first = Tim | last2 = Pope | first2 = Carey N. | date = 2017 | title = Pyridostigmine ☆ | journal = =J. Med. Chem. | url = https://linkinghub.elsevier.com/retrieve/pii/B978012801238397627X|language=en| publisher = Elsevier| pages=B978012801238397627X|doi=10.1016/b978-0-12-801238-3.97627-x|isbn=978-0-12-801238-3}}</ref> * [[huperzine A]] (crosses blood-brain barrier){{Citation needed}} * galantamine - A central/peripheral AChE inhibitor. While prescription only in some countries, galantamine is available over the counter in the United States. * blueberries<ref>{{Cite journal | last = Papandreou | first = Magdalini A. | last2 = Dimakopoulou | first2 = Andriana | last3 = Linardaki | first3 = Zacharoula I. | last4 = Cordopatis | first4 = Paul | last5 = Klimis-Zacas | first5 = Dorothy | last6 = Margarity | first6 = Marigoula | last7 = Lamari | first7 = Fotini N. | date = 2009-03-17 | title = Effect of a polyphenol-rich wild blueberry extract on cognitive performance of mice, brain antioxidant markers and acetylcholinesterase activity | url = https://www.ncbi.nlm.nih.gov/pubmed/19056430 | journal = Behavioural Brain Research | volume = 198 | issue = 2 | pages = 352–358|doi=10.1016/j.bbr.2008.11.013|issn=1872-7549|pmid=19056430}}</ref> == Research studies related to ME/CFS == * 2004, Acetylcholine mediated vasodilatation in the microcirculation of patients with chronic fatigue syndrome<ref>{{Cite journal | last = Spence | first = V.A | author-link = Vance Spence | last2 = Khan | first2 = F | author-link2 = Faisel Khan | last3 = Kennedy | first3 = G | author-link3 = | last4 = Abbot | first4 = N.C | author-link4 = | last5 = Belch | first5 = J.J.F | author-link5 = | date = Apr 2004 | title = Acetylcholine mediated vasodilatation in the microcirculation of patients with chronic fatigue syndrome | url =https://linkinghub.elsevier.com/retrieve/pii/S0952327804000134 | journal = Prostaglandins, Leukotrienes and Essential Fatty Acids|language=en | volume = 70 | issue = 4 | pages = 403–407|doi=10.1016/j.plefa.2003.12.016|quote=|via=}}</ref> - [[pubmed:15041034|(Abstract)]] == See also == *[[Autoantibody]] *[[Vagus nerve]] *[[Vagus nerve infection hypothesis]] ==Learn more== *2003, [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1430829/ The Cholinergic Anti-inflammatory Pathway: A Missing Link in Neuroimmunomodulation], Molecular Medicine, 2003 May-Aug; 9(5-8): 125–134. *2011, [https://www.youtube.com/watch?v=n8j3BWeMOuo Video - "Is acetylcholine toxicity the cause of CFS?"] *24 February 2015, [http://www3.imperial.ac.uk/newsandeventspggrp/imperialcollege/newssummary/news_24-2-2015-14-16-10 Scientists uncover new role for neurotransmitter that helps fight infection], Imperial College London News ==References== {{Reflist}} [[Category:Neurotransmitters and hormones]]
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Module:Category handler/config
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Module:Check for unknown parameters
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Module:Citation/CS1
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Module:Citation/CS1/COinS
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Module:Citation/CS1/Whitelist
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Module:Namespace detect/config
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