Talk:GABAA-rho receptor

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I took the liberty of moving GABA C receptor to GABAC receptor since that way the proper name can show up in the title with the {{downsize}} template. I assumed that this would be an uncontroversial move and that there would be no problems with it, but if there are definitely let me know. Thanks, delldot | talk 03:26, 14 February 2007 (UTC)


I noticed that some of the text in the article was a copyright violation from here. I tried to reword or remove all of the copyvio content I found, but I may have missed some. Also, I'd appreciate it if someone could check to determine whether my rewording is far enough from the original that it's not a problem anymore. The material was in the section entitled "GABAC receptors". Thanks, delldot | talk 04:13, 14 February 2007 (UTC)


Excellent work expanding and cleaning up the page, Boghog2! I took down the tootechnical tag and made a few other tweaks as well. Here is one sentence I thought was still pretty technical (though, admittedly, we're dealing with a very obscure subject here, so some of that can't be avoided):

In contrast to the fast and transient chloride current elicited from GABAA, GABAC receptors mediate slow and sustained responses.

I think we could make stuff more accessible by just defining our terms for the lay reader.

Also, I noticed that some info was removed, e.g. the "genetics" section. I was curious why it was removed, since it seemed like ok info to me. If the reason was that it was too technical, maybe we could reword the material rather than removing it outright. Would it be OK to add it back in? Anyway, thanks for the fixup, Boghog2! delldot talk 18:18, 17 May 2007 (UTC)

  • Per your suggestions, the sentence that describes the differences between GABAC and GABAA chloride current characteristics has been reworded. Also a revised form of the genetics section has been re-added. Thanks for the helpful suggestions Delldot! Boghog2 06:23, 18 May 2007 (UTC)


I'd like to note that this article is diverging a long way from WP:MEDRS, which favors review papers as sources over primary research publications. The problem with primary sources, as long experience shows, is that they make articles very difficult to maintain over the long term. Experience also shows that once an article starts going astray in this respect, the problem tends to get worse and worse over time. I'm not asking for immediate changes but rather for a shift in philosophy here. Looie496 (talk) 16:07, 17 May 2009 (UTC)

While there is a general preference for citations to secondary sources for Wikipedia articles that goes beyond the scope of WP:MED, I believe the necessity for secondary sources in medical related articles is more acute than in other fields. This is especially for true for clinical trials where different studies often give contradictory results. Review articles which compare and contrast the results of different trials are especially valuable. The preference for secondary sources I think has more to do with reliability than maintenance (although the former would certainly have an impact on the latter). This particular article is more within the scope of WP:MCB than WP:MED, hence the preference for secondary sources is less strict. I would like to point out that currently 11 (references # 2, 3, 4, 6, 14, 15, 16, 17, 18, 19, 25) out of 27 citations in this article are to reviews which IMHO is a fairly high percentage. In addition, all of the citations are publications in peer reviewed journals which increases the reliability of these citations beyond other primary sources. Boghog2 (talk) 18:50, 17 May 2009 (UTC)


Would pharmacological agents exploiting this receptor be subject to the same tolerance effects as those which use the GABA-A receptor (e.g. traditional benzodiazepenes)? If not, please provide an explanation and a source. This would be useful to know. Relatedly, there is talk of a non-addictive drug (emapunil), which is a novel mitochondrial benzodiazepine receptor (MBR) ligand. See: Maybe start a new page on this? --1000Faces (talk) 07:52, 17 January 2010 (UTC)

Interesting question. First of all, just to clarify, the target of emapunil and XBD173 is the translocator protein (also known as the peripheral benzodiazepine receptor or the mitochondrial benzodiazepine receptor). The potential of these drugs to have less side effects than benzodiazepines that act through the GABAA receptor is briefly mentioned here. The mechanism of action of classical benzodiazpines and these newer translocator protein ligands is completely different and therefore it is possible that the later will have less addiction potential. However these are very recent research results and as far as I know, there is no definitive evidence as yet to prove or disprove that these drugs will have less addictive potential in humans. Cheers. Boghog (talk) 08:57, 17 January 2010 (UTC)