Talk:Nicotinic acetylcholine receptor

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September 2021

The nicotinic acetylchoilne receptor (nAChR) page appears comprehensive at first glance, however, once each paragraph is dissected, the lack of cohesiveness and relevance is quite evident. One good example is the "effects" subsection. The title of the subsection itself is vague. Is the article referring to the effects of a synthesized agonist or antagonist binding to the receptor? Or the effects of endogenous acetylcholine binding? Nicotine was mentioned however the purpose is unclear. This subsection also lacks a citation, and should be removed completely. In replace of this, the article could be improved with the addition of clinically relevant information about new molecules or drugs in the clinic that target nAChRs. Or a section breaking down individual brain areas that contain different densities of each subgroup of nAChRs and their physiological importance. ````

November 2011

Have added information regarding the molecular mechanism of chnnel opening and blockage described by NMR studies using alpha bungarotoxin as well as normal modes analysis. Coould be even further improved for a better page — Preceding unsigned comment added by 24.59.204.17 (talk) 01:10, 17 December 2011 (UTC)[reply]

May 2011

Have changed the information regarding binding sites as the subunit interface mentioned was incorrect, and have changed it to be more in keeping with what are widely regarded as the involved interfaces in binding and cited literature as such. —Preceding unsigned comment added by 77.103.13.118 (talk) 13:57, 5 May 2011 (UTC)[reply]

February 2010

In Effects, removed other as nAChRs are not voltage gated themselves, therefore 'other' channels are. —Preceding unsigned comment added by 138.38.192.123 (talk) 13:23, 12 February 2010 (UTC)[reply]

Also, the comment about paracrine transmission needs to be removed or updated. Due to acetylcholinestaerase activity, ACh can NEVER act in a paracrine manner. This is not made clear and one wonders how this hypothesis was reached. —Preceding unsigned comment added by 138.38.192.123 (talk) 13:27, 12 February 2010 (UTC)[reply]

This article is dreadful! Even the linked article about nAChR agonists has more information in it about these receptors! See link: http://en.wikipedia.org/wiki/Drug_Discovery_and_Development:_Nicotinic_Acetylcholine_Receptor_Agonists The framework of this article is a disaster, there is no mention of how receptors become desensitised, yet desensitisation is mentioned as if anybody knows about it, there is no inclusion of the Changeux models as diagrams, nothing to highlight the importance of transmitter release (ie where is dopamine?!, the very proposed key molecule increased by nicotine in tobacco smoke via these receptors!). The headings need to be removed or combined, very little is learnt between 'binding' and 'opening'. —Preceding unsigned comment added by 138.38.192.123 (talk) 13:38, 12 February 2010 (UTC)[reply]

January 2010

Reference 2 is incorrect and regards GABA and glycine receptors only. The basis of binding sites on nAChRs is not established in this article. —Preceding unsigned comment added by 138.38.169.72 (talk) 08:39, 5 January 2010 (UTC)[reply]

December 2009

This article says nothing about the difference between alpha and beta subunits! Why bother mentioning something which is not explained? —Preceding unsigned comment added by 138.38.192.59 (talk) 12:42, 10 December 2009 (UTC)[reply]

Semptember 2006

Nice article! --Enigma 05:22, 28 March 2006 (UTC)[reply]

How does Chantix (Varenicline) fit in?

The smoking cessation aide

Chantix pdf

RonEJ / _talk 02:20, 13 April 2007 (UTC)[reply]

Only one type of NAChR?

The opening paragraph states that there is only 1 type of NAChR.

The antibodies to the NAChR at the neuromuscular junction found in Myasthenia Gravis do not affect the NAChR's in the ANS ganglia. Doesn't that imply that there is more than one type? Is it just subunit re-arrangement, like how some permit Ca++ flux and some don't? Hnc 04:00, 16 April 2007 (UTC)[reply]

List of Agonists, Partial Agonists, and Antagonists?

I think that it would be useful to have a list of various molecules that act on nAChRs on this page. Shanata 08:50, 1 November 2007 (UTC)[reply]

Changes

The article is unfinished, please allow relevant changes to be made —Preceding unsigned comment added by 138.38.26.59 (talk) 11:32, 15 September 2008 (UTC)[reply]

October 2008

Resolved

– according to Shanata. Xasodfuih (talk) 12:12, 1 March 2009 (UTC)[reply]

Please can Wonnacott 1997 title in references get its link back instead of only linking via the PMID number? Most people don't think to click on the PMID. The title used to have the link also, please put it back. —Preceding unsigned comment added by 138.38.26.187 (talk) 14:46, 22 October 2008 (UTC)[reply]

Outdated

The exact role of α7 and β2 in nicotine dependence is explained in this paper. I don't have time to update the wiki article, so I just marked it as outdated. Xasodfuih (talk) 06:53, 22 December 2008 (UTC)[reply]

I think that the outdated comment could be removed. The 'Structure' section now contains more information about muscle versus neuronal type receptors, and specifically mentions (α7)₅ receptors and both stoichiometries of the β2-containing (α4)₃(β2)₂ and (α4)₂(β2)₃ receptors. Since there are thousands of researchers worldwide working on nAChRs, we'd have to have the page permanently marked as outdated if we want all of their research to be reflected here. But I do agree that the article needs a nicotine dependence/addiction section. Shanata (talk) 10:40, 2 March 2009 (UTC)[reply]

Fine, it was meant to be just a re minder. I'm happy you're working on the article. Before nobody else was, so the tag achieved its goal :-) Xasodfuih (talk) 11:02, 2 March 2009 (UTC)[reply]

"Coolest receptor ever"

This bit of trivia has been removed [1] by User:Celebere. I cannot find a reference for it myself. At the end of that paragraph a 2008 textbook is cited (Neuroscience. 4th ed. by Purves et al.) Maybe someone can check if the sentence was from that book? Xasodfuih (talk) 06:22, 2 January 2009 (UTC)[reply]

Agonist Binding

As of now, the article states that the agonist must bind for the channel to be open. Unliganded gating has been observed so it may be better to state the the ligand drastically increases the probability of being open. However, I cannot think of an elegant way to word this. — Preceding unsigned comment added by 130.126.48.228 (talk) 20:54, 7 August 2013 (UTC)[reply]

Could you also please indicate a source? One that I could find is associated with mutations.^[1] Maybe, one can add this information in a mutation section. William Savalto (talk) 15:13, 23 March 2021 (UTC)[reply]

References

^ [Purohit, P., & Auerbach, A. (2009). Unliganded gating of acetylcholine receptor channels, Proceedings of the National Academy of Sciences, 106(1), 115-120. https://doi.org/10.1073/pnas.0809272106]

Isolating nAcHR/ history

I think it would be worthwhile to talk a little about the history of how this was discovered. In addition, how it can be isolated, via the torpedo stingray and the alpha bungarotoxin)

Rincrate (talk) 05:21, 29 September 2015 (UTC)[reply]

[1] [Purohit, P., & Auerbach, A. (2009). Unliganded gating of acetylcholine receptor channels, Proceedings of the National Academy of Sciences, 106(1), 115-120. https://doi.org/10.1073/pnas.0809272106]

[1]