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This is the current revision of this page, as edited by 82.54.123.85 (talk) at 16:45, 4 August 2024 (Missing Ligands section !!: new section). The present address (URL) is a permanent link to this version.

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lack of content

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There's a lack of info on this page. What type of receptor is this? What is the structure of this receptor? How does it signal downstream? What's the relationship/difference/importance between the subtypes? —Preceding unsigned comment added by 137.43.95.210 (talk) 19:01, 4 February 2009 (UTC)[reply]

Deleted section implying that mu1 activation does not cause respiratory depression and that mu2 activation does not cause analgesia. Only reference was a page from "opioids.com" referring to a book printed over ten years ago. If they can find peer reviewed evidence that mu1 agonists do not cause respiratory depression (ha, ha), I think it should remain gone. Sakurada et al 1999 Differential involvement of μ-opioid receptor subtypes in endomorphin-1- and -2-induced antinociception, European J Pharm for one showed that mu2 are involved in analgesia.

edit: in fact, it looks like the page doesn't even mention the putative mu1 and 2 subtypes. Whoever wrote that part didn't understand the format of the table and thought there were 6 mu receptors, each with a different specific function! Isn't anyone watching this article? —Preceding unsigned comment added by 160.62.4.10 (talk) 15:50, 1 April 2008 (UTC)[reply]


In fact, this whole page could do with a rewrite by someone more in touch with the opioid field; I'd do it but I don't have the time right now. This article is filled with inaccuracies and relies disproportionately on this concept of mu receptor subtypes which are not widely considered important and are largely based on ancient binding work from one lab. If someone is watching this article I strongly advise it be flagged "needs editing" or whatever denotes a bad article. Scientific articles on wikipedia should be held to a better standard than this. 160.62.4.10 (talk) 15:21, 3 April 2008 (UTC)[reply]


I don't know anything about this field myself, and I found it very technical in nature. What I've noticed is that many articles that are inherently technical also have information that is easier to understand for the everyday person. So in the end I only recognized a little bit of what this article was talking about, but if somebody knows more about it I'm sure they could make it more readable for people not in this field. --shenron (talk) 18:01, 13 April 2008 (UTC)[reply]


In the last paragraph we have a statement claiming that naloxone and naltrexone are inverse agonists and not opioid receptor antagonists. I don't believe this is true, and can find nothing to support this. Naltrexone is given long-term for opioid addiction and the patients receiving it do not experience any "inverse opioid" effects, as far as I can find. I believe they may appear to act as an inverse agonist by precipitating withdrawal in opioid-dependent individuals upon administration, but in opioid-niaeve individuals naloxone should have little to no effect. The body has natural opioid peptides like endorphins that bind to these receptors, and naloxone can block these as well which would lead to an inverse agonist effect, but I sincerely doubt the drug itself is an inverse agonist. I believe whomever added this last statement has "receptor antagonist" and "inverse agonist" backwards. I've added a citation needed marker at the end of this paragraph. —Preceding unsigned comment added by 66.225.223.4 (talk) 18:51, 25 August 2009 (UTC)[reply]

Genetic polymorphism

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This is an interesting possibility that can be worked into the article if we can find some other citations: Nagashima M, Katoh R, Sato Y, Tagami M, Kasai S, Ikeda K (2007). "Is there genetic polymorphism evidence for individual human sensitivity to opiates?". Curr Pain Headache Rep. 11 (2): 115–23. PMID 17367590. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link) MeekMark (talk) 14:23, 13 November 2009 (UTC)[reply]

Objection to rename

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This page was moved from "Mu Opioid receptor" to "M-opioid receptor". I object to this move, because the other opioid receptor subtype pages are not named in this way, and the "M" nomenclature is non-standard. Therefore, I am going to revert the move, to "mu Opioid receptor". Please note that we name delta Opioid receptor and kappa Opioid receptor the same way. --Tryptofish (talk) 21:23, 7 January 2011 (UTC)[reply]

Inclusions

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I have added the propiram derivatives because it is only the matter of 2 sentences (including links) but things like nexeridine DID reach the market so does that metic inclusion? I put the viminol derivatives in the READ section and someone else added it to the article. Nexeridine overlays dextropropoxythene (and it's pyridyl derivatives) so it does provide a path for students to follow. Should it have a page? — Preceding unsigned comment added by 81.99.74.135 (talk) 18:06, 11 September 2018 (UTC)[reply]

Ligands?

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Compare to δ-opioid receptor and κ-opioid receptor. This article does not have a list of ligands. Kimen8 (talk) 23:20, 10 December 2023 (UTC)[reply]

Missing Ligands section !!

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Ligands ?? 82.54.123.85 (talk) 16:45, 4 August 2024 (UTC)[reply]