Talk:GABAA receptor

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Contents 1 human body --> brain 2 ??? 2.1 Condensation? 3 Move 4 Benzodiazepine receptor != GABAa receptor 5 topiramate

[edit] human body --> brain

I changed this sentence from the introduction because glycine is the major inhibitory neurotransitter in the spine, not GABA. Moez ^talk 23:44, 20 June 2006 (UTC)

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This article may be too technical for a general audience. Please help improve this article by providing more context and better explanations of technical details to make it more accessible, without removing technical details.

38.100.34.2 16:56, 12 April 2007 (UTC)

[edit] ???

Is that the text from a thesis or something ? ^talk 19:33, 30 November 2006 (UTC)

[edit] Condensation?

This article seems like a very well-researched paper, but I wonder if it too long and detailed for Wikipedia. Would anyone object some major culling? Alki 17:49, 2 December 2006 (UTC)

Thank you, this article as been reported to the WP:Extra-Long Article Committee and may have copyvio issues. We are investigating this. --Sadi Carnot 19:21, 6 December 2006 (UTC)

[edit] Move

I've taken the liberty of moving GABA A receptor to GABAA 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 02:13, 12 February 2007 (UTC)

[edit] Benzodiazepine receptor != GABAa receptor

The benzo receptor is not the same as the GABAa receptor! The GABAa receptor has different spots for different ligands, and the receptor site for GABA is different than the site for benzos, although both sites are both on the same receptor protein complex (not necessarily the same protein subunit). This is a very important distinction. If the benzos bound to the same site as GABA, they would presumably have effects similar to, or the same as the endogenous ligand (GABA). In reality, the benzos actually act as allosteric ("other site") GABA modulators by altering the GABA receptor protein's conformation. In fact, the GABAa receptor protein has multiple receptor sites (which are located on multiple subunits) for a variety of ligands, including barbiturates and certain steroids, and also certain anesthetics. As it stands, this article, as well as many, many others that reference the so-called "benzodiazepine receptor" are incredibly misleading. It is the benzo receptor site on the GABA_A receptor complex. See figure 6 on the following page [1] and also [2]. I also have several textbook references that I will add as soon as the article has been changed to reflect this subtle but important difference. Fuzzform 01:16, 28 September 2007 (UTC)

In fact, this article would do better to be named "GABA_A receptor complex". It really is a complex, as it binds multiple ligands in multiple spots around the ion channel, and is made up of multiple subunits (i.e. it is in it's quaternary structure). Fuzzform 01:20, 28 September 2007 (UTC)

• I agree that we should make clear that GABA and benzodiazepine ligands bind to different sites on the GABA_A receptor complex. However the term "receptor" not only refers to the binding site on the protein, but also to the entire protein or protein complex (which would include allosteric binding sites). For example, the gene (and protein encoded by the gene) for GABRA1 is called the "gamma-aminobutyric acid (GABA) A receptor, alpha 1". The reason for this of course is historical. Ligands for many receptors including the GABA_A receptor were discovered before the protein was isolated and characterized. Hence the protein was named after the ligand that bound to it and the name stuck even after the gene/protein was cloned and sequenced. Hence the distinction that you are proposing is in my opinion a semantic one. Cheers. Boghog2 07:15, 4 October 2007 (UTC)

[edit] topiramate

A recent study has shown that use of topiramate has reduced drinking events in alcholics attempting to quit drinking. I looked into the mechanism of action of topiramate and discovered that it also affected the GABAA receptor in a fashion that wasn't blocked by flumazenil. The theory was that this had something to do with its anti-seizure effects. I suspect it also may have something to do with its common side effect of drowsiness and morning hangover feeling.

My question is: topiramate also has some effect in reducing frequency and severity of migraine headaches and decreasing carbohydrate cravings. The latter can actually lead to weight loss. Would this be a possible effect of its actions at the GABAA receptor, or is it more likely due to its effects of antagonizing kainate activation of the kainate/AMPA subtype of the glutamate receptor? —Preceding unsigned comment added by Samuraidoctor (talk • contribs) 13:43, 10 October 2007 (UTC)