Talk:Muscarinic acetylcholine receptor
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Article created
[edit]I've been studying the autonomic nervous system, and particularly the various ACh receptors and the drugs and substances, for alzheimers, parkinsons, IBS, cardiac drugs, bronchodilators, etc, background for famous drugs like scopolamine/atropine because this needs to be written and existing stuff tied together in Wikipedia and it struck me as a current weakness. I'm starting with muscarinic receptors, and hope to edit nicotinic receptors, and to a lesser extent, ach, sympathetic/parasympathetic/autonomous nervous system atropine/scopolamine, and to crete pages for dicycloverine/milverine/cimetropium etc, etc. This will take some time though.... Kaet 03:44, 8 Sep 2004 (UTC)
Hopefully you will forgive me using this discussion page to note some research which will be valuable in future (to myself, or some other poor sod), but which don't yet fit into the article itself.
- m1: not PTX, not CTX, G_q,G_i, slow EPSP at ganglion1, secretory glands23, cns23. IP3
- m2: PTX sensitive, not CTX, G_i,G_o,G_z, IPSP at ganglion1, smooth muscle13, myocardium2, cns23. -cAMP3
- m3: not PTX, not CTX, G_q,G_i, smooth muscle123, secretory glands23, cns23. IP release3
- m4: PTX sensitive, G_i, G_s? (would be CTX for G_s), smoothmuscle2, secretory glands2, cns23, -cAMP3
- m5: not PTX, cns3. IP3
Sorry about the delay half way through expanding this page. Caused by a work crisis. Should resume shortly. kaet
- Hi, Kaet. I have expanded and edited the Parasympathetic page, if there is anything missing feel free to add it. Also, i am willing to help you out on your mass editing. =) see you around. --LowLifer 06:58, 4 October 2005 (UTC)
- Added in "Also see Tiotropium". I am just a patient that uses the drug and I came to the conclusion it seems to block the nicotine (darn cigarettes) and open my airways. I have no ego to bruise so feel free to clean up.
- Thank you for creating this article. It is awesome. I read it several times a year. It is one of my favorites. Stephen Charles Thompson (talk) 00:20, 14 January 2013 (UTC)
Done
Agonists and antagonists - go specific
[edit]Hello. the agonists and antagonists listed in the table should be more specific to the receptor, otherwise it makes no sense and we can simply write Acetyl choline in each one. So I've inserted specific agonists and antagonists for each receptor.vineetcoolguy 12:30, 19 August 2007 (UTC)
- I would like to see the the affinity each agonist and antagonist has on each of the muscarinic receptor types. I don't simply want to know if an agent has an effect, I want to know how effective each of these agents are. I want to see how selective certain agents are on various receptors. Stephen Charles Thompson (talk) 03:01, 14 January 2013 (UTC)
"Atropine (To Dilate The Pupil)"
[edit]The sentence which reads "atorpine (to dilate the pupil) should be changed. Although atropine can and was once used to dilate the pupil in earlier times for cosmetic reasons, it is no longer used for this application and we realise the dangers of doing so. It should be noted there however that atropine is used in the clinic, especially emergency medicine where it is used to block the effects of organophosphate poisoning, increase heart rate and cardiac contractility and increase blood pressure. It is named on the World Health Organisations list of essential drugs for the emergency department resuscitation room. —Preceding unsigned comment added by 152.78.249.51 (talk) 10:38, 15 March 2009 (UTC)
muscarinic receptors on sweat glands
[edit]the muscarinic receptors on sweat glands has inhibitory effect or excitatory effect on erector muscle? Which I mean the muscarinic receptors causes ( of course by secondary messenger ) the ligand-gated potassium channel to open ( IPSP ), or the ion channel to opens, allowing K+, Na+, Ca+2 to diffuse through ( EPSP )? Thanks a lot.
There is no mention of glycopyrrolate (Robinul) anywhere in the article
[edit]Due to the fact that atropine has overwhelmingly been replaced as the anticholinergic of choice for prevention of neostigmine induced bradycardia, it should be included for completeness. There are articles (Ramamurthy et. al., 1972; Klingenmaier et. al., 1972; Mirakhur et al., 1981; etc...) in the literature dating back to the early 1970s citing the advantages of glycopyrrolate over atropine for reversal of neuromuscular blockade. Until it is included, this article is incomplete.24.178.161.29 (talk) 01:09, 31 March 2011 (UTC)
A mushroom?
[edit]Seriously people. A mushroom? Can someone find a better image that can be used as a visual representation of a Muscarinic acetylcholine receptor? --68.38.75.142 (talk) 15:28, 26 October 2012 (UTC)
- The mushroom is a perfect symbol. It has historical significance as being one of the first known external sources of acetylcholine and our awareness of a parasympathetic system in the human body. Our stone-age ancestors may not have had specific concepts about Muscarinic receptors or cranial nerves but they did know the very specific effects of this mushroom, and the opposite effects of the antagonists found in Henbane, Jimsonweed / Datura, Belladonna / Nightshade. Stephen Charles Thompson (talk) 00:14, 14 January 2013 (UTC)
Done
Hyoscscyamine
[edit]Hyoscscyamine is a notable muscarinic antagonist like atropine yet it is not referenced here. The Hyoscyamine article states that "at comparable doses, hyoscyamine has 98 per cent of the anticholinergic power of atropine", but no citation is provided. If someone (including myself) were to find a reference for this, we should update both of these articles accordingly. Stephen Charles Thompson (talk) 23:59, 13 January 2013 (UTC)
- The best I have been able to dig up are pharmaceutical references like this one, presumably prepared for insertion in prescription fulfillments.[1] Note: this is released according to the freedom of information act.
It states that it is an anticholinergic agent. It does not specifically state which receptor type it acts upon but does infer this information by describing the sites where the effected receptors are. "Hyoscyamine sulfate inhibits specifically the actions of acetylcholine on structures innervated by postganglionic cholinergic nerves and on smooth muscles that respond to acetylcholine but lack cholinergic innervation. These peripheral cholinergic receptors are present in the autonomic effector cells of the smooth muscle, cardiac muscle, the sinoatrial node, the atrioventricular node, and the exocrine glands. At therapeutic doses, it is completely devoid of any action on autonomic ganglia. Hyoscyamine sulfate inhibits gastrointestinal propulsive motility and decreases gastric acid secretion. Hyoscyamine sulfate also controls excessive pharyngeal, tracheal and bronchial secretions." Stephen Charles Thompson (talk) 03:26, 14 January 2013 (UTC)
- This description specifically coincides with M1, M2, M3 receptors. I am unable to make any connection between this description and M4 or M5 receptors and have therefore omitted them. Anyone out there have a scientific journal to back this up? Stephen Charles Thompson (talk) 03:47, 14 January 2013 (UTC)
Fix this!! Wikipedia says Atropine is a Muscarinic on one page and an anti-Muscarinic on another. For the love of the Lord. http://en.wikipedia.org/wiki/Anticholinergic http://en.wikipedia.org/wiki/Muscarinic_acetylcholine_receptor — Preceding unsigned comment added by 64.134.227.97 (talk) 05:08, 5 January 2014 (UTC)
References
- ^ EDWARDS PHARMACEUTICALS, INC.; BELCHER PHARMACEUTIALS, INC. (May 2010), U.S. National Library of Medicine http://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=f33a4774-9fbb-4782-a7e1-068e83b7504d, retrieved January 13, 2013
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Unsourced information - M1 and M2 in autonomic ganglia - "Recovery receptors"
[edit]Could anybody find a source for this article's claim that the M2 receptor mediates a "recovery" via hyperpolarisation of postganglionic cells in the autonomic ganglia? (Or even that M2 is localised to autonomic ganglia?)
As for M1-mediated slow EPSP in the autonomic ganglia, the only reference appears to be a faculty website at the University of Toledo that has since been taken down. Anybody able to find primary literature for this?
This uncited (and potentially misleading) information has been in this article for almost as long as it has existed.
And the remainder of the section on "recovery receptors" consists almost exclusively of nonspecific information about the cholinergic system and autonomic NS; I do not believe it belongs in this article.
134.173.78.1 (talk) 07:06, 8 October 2014 (UTC)
Well, I was able to retrieve the one citation given for M1-mediated "slow" EPSP from Archive.org (the aforementioned faculty web page -- hardly a reliable source), and -- surprise! -- nothing whatsoever in there about "slow" EPSP or about muscarinic receptors in the autonomic ganglia. (See https://web.archive.org/web/20080401042754/http://www.neurosci.pharm.utoledo.edu/MBC3320/acetylcholine.htm )
I would then strongly recommend removal of the entire "Recovery Receptors" section from this article unless reliable citations can be identified.
134.173.78.1 (talk) 07:44, 8 October 2014 (UTC)
Assessment comment
[edit]The comment(s) below were originally left at Talk:Muscarinic acetylcholine receptor/Comments, and are posted here for posterity. Following several discussions in past years, these subpages are now deprecated. The comments may be irrelevant or outdated; if so, please feel free to remove this section.
Recovery Receptors.
Has anyone else noticed the style of writing in this section? There's use of 'i' in a sentence, saying, "i am wondering..." which doesn't seem appropriate for Wikipedia's standard. Most of the sentences begin with 'the' also uncapitalized. I'm not much of an expert on Muscarinic ACh receptors but this makes me feel that the page is less reliable... Acemonvw (talk) 20:18, 1 March 2009 (UTC) Well, actually, looking back, it appears that someone was just trying to figure out the best way to categorize this page, but it seems like within the page is not the best place to try to discuss these changes. Acemonvw (talk) 20:22, 1 March 2009 (UTC) |
Last edited at 20:22, 1 March 2009 (UTC). Substituted at 00:38, 30 April 2016 (UTC)
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