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Archive 1

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It is interesting to note that the easiest representation of gamma-aminobutryic acid has no availability to attach a side-chain (or 'R') in a different place to the alpha amino acids [a separate group of amino acids]. — Preceding unsigned comment added by Rachelmargaretorr (talk • contribs) 11:26, 9 January 2011 (UTC)

Nicotine affect GABA

It seems that nicotine affect GABA och decrease its effect. See for example:

http://www.sciencedaily.com/releases/2007/12/071208092505.htm

http://jp.physoc.org/cgi/content/abstract/536/1/89

Before my edit

I'm surprised not to see any mention of alcohol in the list of drugs which can affect GABA. GABA movement is affected both in FASD and in direct drinking of alcohol.


"So far three general classes of GABA receptor are known, more than one of which is often represented in the same organisms. These include both so-called ionotropic receptors, which are ion channels themselves, and metabotropic receptors, which are G protein-coupled receptors that open ion channels via intermediaries (G proteins)."

Which is the third type? —The preceding unsigned comment was added by 24.211.134.8 (talk • contribs) .

Scroll down two paragraphs: The 3 types are GABA A receptor, GABA B receptor and GABA C receptor. A and C are ionotropic, B is metabotropic. -- PFHLai 03:16, 27 September 2005 (UTC)

Effects on GABA on hGH production

There are some advertisments of GABA supplements claiming GABA instructs the brain to produce more Human Growth Hormone during deep sleep. Any thoughts?

Advertisements claim all sorts of stuff. Any GABA you would ingest will be broken down by your digestive system way before it will ever get to your brain. Nrets 19:54, 14 March 2006 (UTC)

el acido gamma mini butirico(gaba)es un neuro transmisor y no es totalmente destruido por el sistema digestivo,soloq ue no ejerce su accion igual que en condiciones normales.Dr.Ricardo Garcias Puentes.Profesor titular.Espacialista en Medicina Interna Segundo Grado.Cuba.

better name

Should it be called Gamma-aminobutanoic acid? That is all I have ever heard it called, and it seems more accurate and consistant. 195.194.89.7 15:52, 2 March 2006 (UTC)

Gamma-aminobutyric acid is correct. Nrets 19:54, 14 March 2006 (UTC)
The IUPAC name is 4-aminobutanoic acid as stated in the infobox on the rhs of the article. It is usually referred to as Gamma-aminobutyric acid though. 83.147.180.185 18:58, 8 August 2007 (UTC)

Requesting more info on human effects (e.g. emotions, physical activity) of increased or decreased GABA

As opposed to just the physiological processes involved with it please

Is GABA omni-present/ pervasive? If so, how is it transported? By blood; CSF; or Glial tissue? Does it change in strength, say in sync with the Circadian rhythm? Don Nicol 11:30, 06 Jul 07

GABA is released by GABAergic neurons (usually interneurons). It is transported in the same way as any other neurotransmitter (glutamate for instance). GABAergic neurons are indeed found everywhere. Without them the brain would be in a nearly constant epileptic state. I expect it changes both in degree of postsynaptic effect and in overall tonic levels over time, the former due at least in part to modulatory affects and the latter due to the fact that activity levels in general change with state (e.g. sleep vs. resting vs. active). digfarenough (talk) 20:47, 6 September 2007 (UTC)

GABA supplements

Considering how regulated and addictive GABA-affecting drugs like barbiturates and benzodiazepines are, I was very surprised to find that GABA is legally available as a supplement from online health stores (eg [[1]]). Is there any sort of clinical study or official statements on how well (if at all) these work for relieving anxiety, or whether or not they create any sort of dependency or tolerence effects like those drugs? 69.85.180.131 07:56, 10 November 2006 (UTC)

My guess is that taking GABA orally will do absolutely nothing because it is unlikely to cross the blood-brain barrier and significantly interact with GABA receptors. But whether or not their products work at all doesn't matter in the supplement industry.
That is indeed correct, GABA does not cross the blood brain barrier. However, it does have peripheral effects, and this may account for its use as a supplement. This may be worth mentioning in the article, as it does seem fairly widespread in use. Fuzzform 03:13, 2 April 2007 (UTC)

This comment is entirely anecdotal, but GABA is thought to help some forms of ADD or ADHD. My daughter (now 10) has always been overactive, over focused, like her mainspring is wound too tight. She is alway thinking about what she wants to do and instantly frustrated and angry by anything (whether internal or external) that thwarts her ability to accomplish her goals. Totally unable to relax, to the point of being almost constantly just short of a state of panic.

On GABA (750mg twice a day) she is calm, relaxed, has a great sense of humor, and seems to become a normal kid. If she is taken off of GABA for 24 to 48 hours, she turns back into this angry hyper over-focused kid again. I don't know the chemistry, but I know that GABA is doing great things for my daughter, and having watched the effects for over a year, I have to believe that GABA does have some fairly direct effect on the brain. Be glad to communicate with anyone about my experiences, and would also be glad to have any thoughts about problems with a 10 year old taking GABA. I did not start her on this drug without a lot of forethought. Thanks GALJohnson (talk) 14:28, 10 September 2010 (UTC)

  • GABA-fortified foods are apparently big in Japan [2]. According to Abdo AM et al 2006, oral GABA induces relaxation, antianxiety effects, and increased IgA in the saliva. However, the first author seems to be employed by the manufacturer of a GABA supplement. They don't mention the blood-brain barrier issue, but do note that brain waves changed after GABA supplementation. II | (t - c) 22:09, 8 June 2009 (UTC)
  • The " supplement industry " claims, GABA has an influence on the pituitary gland, which controlls the level of HGH.

" The hypothalamus is bounded in part by specialized brain regions that lack an effective blood-brain barrier; " ( Hypothalamus ) . Even I am convinced, GABA has no effect on HGH - levels in blood ( because no one ever said how exactly it influences the pituitary gland ) , the argument, GABA cannot have an influence on the HGH - level, because it cannot pass the blood-brain-barrier, in my oppinion is questionable, because it just does not need to pass the blood-brain-barrier. Skalarido

There is a good review on the subject: Müller EE, Locatelli V, Cocchi D (1999). "Neuroendocrine control of growth hormone secretion". Physiol. Rev. 79 (2): 511–607. PMID 10221989. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link). This paper states that GABA does not cross the BBB, but even if it could there is no evidence that it has a stimulatory effect on GH production - it appears to have both stimulatory and inhibitory effects, depending on the physiology of the individual. I've updated the article to reflect this.--Amaher (talk) 04:24, 19 January 2010 (UTC)

Is GABA transaminase used to produce GABA?

I've read that "However, GAD is not the only source of GABA. The Krebs cycle also serves to synthesize GABA via GABA-transaminase. " --CopperKettle 10:59, 31 December 2006 (UTC)

Check out this[3] page for some interesting info on that topic. Includes very nice picture of biosynthetic pathway that GABA is involved in. Fuzzform 03:19, 2 April 2007 (UTC)

Data rape drug?

I use GABA for insomnia and i have found it works quite well but i had thought i had heard it is used as a date-rape drug.Does anyone know anything about this?

You're probably thinking of GHB, the nitrogenous analogue of GABA. (Ccroberts( t · c · g ) 16:53, 7 July 2007 (UTC))
It's the other way around, GABA is the nitrogenous analogue of GHB. 83.147.180.185 17:24, 8 August 2007 (UTC)
Ooopsie, thanks, that would be gamma-hydroxyl analogue of GABA. (Ccroberts( t · c · g ) 18:53, 8 August 2007 (UTC))

Pharmacology

This section contains some inaccuracies that should be clarified: Avermectins target glutamate-gated chloride channels, not GABA receptors (e.g. Wolstenholme & Rogers, 2005). Opioids and cannabinoids affect GABA signaling indirectly, but not through GABA receptors. I have never heard of many of the other substances mentioned here to interact with GABA receptors, such as carbamazepines, fluoroquinolones or phenytoin - please include references or remove them. Valerenic acid (see Valerian (herb)) should be included (Khom et al., 2007). 193.171.174.141 13:48, 24 May 2007 (UTC)

Acetyl GABA

Why not it could cross the blood brain barrier

"Acetyl GABA" doesn't mean anything - it needs a modifier to describe where the acetyl group would be. Where would you attach the acetyl group, and moreover, why would you want to? You're probably thinking that because acetyl-L-tyrosine, acetyl-L-cartinine, etc., can cross the BBB more easily, that some kind of "acetyl GABA" would do the same. That's unlikely. Anyway, "regular" GABA more than likely has the ability to cross the BBB. Fuzzform (talk) 05:29, 4 April 2008 (UTC)

Dopamine & Serotonine

Im new to this. Does GABA acts as an inhibitor to Serotonin and Dopamine? The article does not spell that out. Further, if one is suffering from to much dopamine, due to withdrawal sympoms of an dopamine antagonist (Zuclopenthixol), whould this help to eliviate acute symptoms, by preventing inhibition? Any reason to not do so? Would using GABA prevent the brain to readjust, or would the withrawal proced as usual, only with lesser sympoms? Would there be any withrawal sympoms from discontinuating the use of GABA? The answer to the questiong could potentialy be very usefull to me. Thanks.--Striver - talk 04:02, 14 February 2008 (UTC)

Both dopamine and serotonin are "neuromodulators," which alter the response to the more classical neurotransmitters glutamate and GABA - glutamate has an excitatory effect on neurons, while GABA is inhibitory. Things get much more complicated, however, with the neuromodulators, since they have different effects depending on the receptor subtypes present on the neuron in question. Dopamine receptors may belong to either the D1-like family, which is excitatory, or the D2-like class which is inhibitory; the same may be said for serotonin receptors (subtypes 1 and 5A are inhibitory while subtypes 3, 4 and 7 are excitatory...2 is even more complex). Add to that the fact that they may have an excitatory effect on an inhibitory interneuron (resulting in a net inhibitory action) and you get the picture of how complicated things can get. Bear in mind also that GABA can not cross the intact blood brain barrier in any meaningful amount. I am not a clinician, but I would guess that while GABAergic drugs might help with some symptoms of zuclophenthixol withdrawal, they would likely fail to address others. A better solution would probably be to taper the dose rather than stopping abruptly, but if you're looking for medical advice you need to see a doctor. St3vo (talk) 19:03, 14 February 2008 (UTC)

Is there any difference from withdrawal sympoms of an dopamine antagonist such as Zuclopenthixol and the effects of an stimulants such as Amphetamine? Would decresing Levodopa levels help to aliviate the problem? Or could spiking Pyridoxal phosphate levels help to lower dopamine levels by forcing it to be created outside the CNS? --Striver - talk 04:06, 14 February 2008 (UTC)

Answer to your first question: no, not really. Second question: most likely. Third: it's a profoundly bad idea to force the body to create dopamine in the periphery. There are drugs that specifically counteract this effect. Also, taking levodopa if you don't have Parkinson's disease is another really bad idea. Compared to the drugs you've mentioned, GABA is completely harmless. Fuzzform (talk) 05:38, 4 April 2008 (UTC)
For a good discussion of Zuclopenthixol and the dopaminergic/serotonergic systems, see this blog post I stumbled upon while researching your questions. Best, St3vo (talk) 21:26, 14 February 2008 (UTC)

"GABA is an amino acid"?

While correct, in biochemistry "amino acid" usually refers to an alpha-amino acid, which GABA is not. So perhaps calling it an amino acid in the first sentence, in the biochemical context of this article, might be misleading.--Mongreilf (talk) 11:59, 21 May 2008 (UTC)

In Purves' textbook Neuroscience, GABA is classified as a (small molecule) amino acid neurotransmitter (page 120). Though, I have to admit that this classification is a bit misleading, due to the fact that "amino acid", used without a qualifier, refers to the alpha amino acids. Fuzzform (talk) 19:33, 1 October 2008 (UTC)

Molecular structure

From Talk:Gamma-Hydroxybutyric acid:

I remember looking at this topic a while ago, and it was complicated. Several papers have been published about the conformation of GABA, and if I remember correctly there were several conformations close in energy, with the preferred one depended a lot on whether you were talking about the gas-phase conformation, the conformation in solution (and in which solvent), or the binding conformation. Of course, there is the issue with the protonation states. And then there's the crystal structure. So, which one do you prefer as the True Structure? ;-) I can send you the CIF with the crystal structure if you want, or if you can get it from the CSD, the code is GAMBUT01, GAMBUT02, GAMBUT04, or GAMBUT10 (each one has a different packing, but the molecule itself looks more or less the same, zwitterionic with a trans NCCC and a gauche CCCC). --Itub (talk) 16:57, 18 June 2008 (UTC)

See also Acta Cryst. (1983). B39, 360-366, The neutron structure of and thermal motion in γ-aminobutyric acid (GABA) at 122 K.

Ben (talk) 17:32, 18 June 2008 (UTC)


GABA as an Excitatory Neurotransmitter in Prenatal Development?

I believe there should be a section or at least expansion of a previous section to include the role of GABA as a control neurotransmitter in the development of neurons as explained in Neuroscience by D. Purves et al Pg. 135 Box 6D —Preceding unsigned comment added by 152.78.249.55 (talk) 19:49, 9 January 2009 (UTC)

Which edition of Purves? This one?
Fitzpatrick D, Purves D, Augustine G (2004). Neuroscience (3rd ed.). Sunderland, Mass: Sinauer. ISBN 0-87893-725-0.{{cite book}}: CS1 maint: multiple names: authors list (link)
Thank you for your suggestion. When you believe an article needs improvement, please feel free to make those changes. Wikipedia is a wiki, so anyone can edit almost any article by simply following the edit this page link at the top. The Wikipedia community encourages you to be bold in updating pages. Don't worry too much about making honest mistakes—they're likely to be found and corrected quickly. If you're not sure how editing works, check out how to edit a page, or use the sandbox to try out your editing skills. New contributors are always welcome. You don't even need to log in (although there are many reasons why you might want to). Cheers. Boghog2 (talk) 20:08, 9 January 2009 (UTC)

It is in the Fourth Edition of Purves, i'm not sure if and where it is in the third edition. —Preceding unsigned comment added by 152.78.249.55 (talk) 09:28, 10 January 2009 (UTC)

OK, here is the complete citation:
Purves D, Fitzpatrick D, Hall WC, Augustine GJ, Lamantia A-S (2007). Neuroscience (4th ed.). Sunderland, Mass: Sinauer. pp. 135, box 6D. ISBN 0-87893-697-1.{{cite book}}: CS1 maint: multiple names: authors list (link)
And another one that seems relevant:
Jelitai M, Madarasz E (2005). "The role of GABA in the early neuronal development" (PDF). Int. Rev. Neurobiol. 71: 27–62. PMID 16512345.
I don't have access to the Purves text book, but I will see what I can do using the Jelitai paper. Boghog2 (talk) 11:30, 10 January 2009 (UTC)
There was already some discussion of the role of GABA in development in the function section of this article. I have subdivided the section in to neurotransmitter and development subsections to more cleanly separate the two roles and expanded the development subsection. Boghog2 (talk) 12:22, 10 January 2009 (UTC)

Article title

Why is the article title "gamma-Aminobutyric acid" rather than "γ-Aminobutyric acid"? --Oldak Quill 14:20, 30 March 2009 (UTC)

Does it matter? Nearly everybody who comes to the article will find it as GABA. Looie496 (talk) 22:19, 30 March 2009 (UTC)

Attempt to create IPA pronunciation

In the first sentence, I've added an IPA pronunciation key for GABA's full chemical name. I'm not fully versed in doing this, so I might have gotten either the convention or symbols wrong. I'd appreciate a second look from someone familiar with it. Thanks. — VoxLuna ☾ orbitland   07:16, 4 April 2009 (UTC)

Hmm, I wonder how helpful that will be. I bet not one person in a million understands that system. Looie496 (talk) 22:13, 4 April 2009 (UTC)
I certainly don't. It took half an hour in the IPA article to devise. I've tried it once before for Countach, where IMHO my spoken exampleⓘ is more helpful than reading "kunˈtɑʧ". Maybe I'll belt one out for this article. — VoxLuna ☾ orbitland   05:48, 7 April 2009 (UTC)


Purge references to GABAC

As of recently, IUPHAR has depreciated the use of the term GABAC. Quite rightly so, and this was just a catch all for non GABA-A non GABA-B receptors, and doesn't belong in the age of moleuclar pharmacology. To quote from the IUPHAR review "[all of the evidence] led to the decision of the Nomenclature Committee of IUPHAR to designate the GABA rho receptors as part of the GABAA-R family and to recommend against the use of the term GABAC receptor."

International Union of Pharmacology. LXX. Subtypes of gamma-aminobutyric acid(A) receptors: classification on the basis of subunit composition, pharmacology, and function. Update. Olsen RW, Sieghart W. Pharmacol Rev. 2008 Sep;60(3):243-60

I'm going to come back when I'm less busy and remove references to the GABAC receptor, apart from to mention the fact that it is a historical curiosity Bilz0r (talk) 21:17, 12 May 2009 (UTC)

Great! Looie496 (talk) 16:12, 13 May 2009 (UTC)
I have made changes that you have suggested both in this article and in GABA receptor article. However what should we do with the GABAC receptor article? I think we should keep it rather than try to merge it with GABAA receptor because of the historical significance and because they are a distinct subgroup of GABAA receptors. But should we rename the GABAC article GABAA-ρ? Boghog2 (talk) 22:26, 13 May 2009 (UTC)
I see no need for a GABAC receptor article. If we were going to have articles for each mistakenly named receptor then we'd be in serious trouble (i.e. articles for all the 5-HT receptors before they were split up, and two for the 1C receptor, once for the old 1C and another for the new 1C receptor, and all of the messing around that went on with GABAB subunits etc...). There would be no end to it. I feel there should be three articles. One on GABA, one on GABA(A) receptors and one of GABA(B) receptors. Within the GABA(A) receptor article, there should be sections on each of the subunit classes (α, β, γ etc) and functional differences of each subtype should be addressed therein. If someone searches GABAC, it should forward them to the section on ρ subunits. Bilz0r (talk) 00:17, 14 May 2009 (UTC)
I respectfully disagree for the reasons that I have already given above and that you have not directly responded to. The term "GABAC receptor" was widely used before the IUPHAR committees recommendation and it would be a serious mistake not to alert the reader that (1) there is frequent reference in the older literature to GABAC receptors and (2) these GABAC receptors are now called GABAA-ρ receptors. Furthermore I do not see the problem of having an article on a distinct subclass of GABAA receptors. If the GABAC receptor article was renamed as "GABAA-ρ receptor" this subclass of receptors would not be misnamed. Boghog2 (talk) 01:58, 14 May 2009 (UTC)
Quoting Chebib M, Johnston GA (2000). "GABA-Activated ligand gated ion channels: medicinal chemistry and molecular biology". J. Med. Chem. 43 (8): 1427–47. doi:10.1021/jm9904349. PMID 10780899. {{cite journal}}: Unknown parameter |month= ignored (help):
  • The two subfamilies [GABAA vs. GABAC/GABAA-ρ] can be distinguished on the basis of their different channel properties, the availability of selective agonists, antagonists, and modulators, the different chromosomal localization of the genes coding for the protein subunits of the two subfamilies and the reluctance of these subunits to coexpress in functional receptors, and the different proteins that anchor the protein complexes to the cytoskeleton.
Based on the above, two seperate articles the first covering GABAA and a second covering GABAA-ρ is clearly justified. Boghog2 (talk) 02:22, 14 May 2009 (UTC)
If it were possible to redirect to a section, I would see this as 50-50, but I don't think that's possible -- so it seems to make sense for the GABAC to clue the reader in to the story and then send the reader to the GABAA-ρ section. Looie496 (talk) 02:16, 14 May 2009 (UTC)
Um, well, I was wrong -- you can redirect to a section; so I see it as 50-50 after all. Looie496 (talk) 02:18, 14 May 2009 (UTC)
The presence of selective agonists and antagonists doesn't mean their should be a seperate page. There are vaguely selective agonists for a huge number of subtype combinations; of which in total there are over 10,000. As I say, there are a huge number of ways to refer to receptors, most of which are historical.
The whole thing makes no sense. GABAA-ρ receptor? ρ what? 1 2 or 3? All receptors containg ρ subunits? Because that is completely different from GABAC receptors, as not all receptors with ρ subunits are GABAC receptors. And if you have a page for GABAA-ρ receptor you need to have one for GABAA-alpha receptor GABAA-beta receptors. The chromosome placing is a complete red hearing, all GABAA subunits are spread over a wide region of the genome. So, to be clear; my reasoning for merging GABAC receptor with GABAA receptor is: The GABAC receptor is a phrase that doesn't make sense in the molecular era, we now know what is causing 99% of those non-bicuculline non-phaflofen responses. ρ homomers containing GABA receptors have been official classified as GABAA receptors. ρ homomers are unusual, but so are delta containing GABAA receptors, alpha4 and alpha6 containing GABAA receptors. alphabeta pentamers are interesting. But we don't have pages for them. We have pages for the subunit.
And then if you argue do have a page for every subunit combination you need to make 10,000 pages. If you then say we need a page for every CONFIRMED receptor, then we still don't have a page on ρ receptors, because we don't know what the ρ homomers are made of? (ρ1)2(ρ2)2(ρ3)? We have no idea.
I might also add that just because it is in old liturature doesn't mean we give it its own page. As I say, we have no page on the 5-HT1C receptor, it forwords straight to the 5-HT2C receptor. Bilz0r (talk) 08:53, 14 May 2009 (UTC)

(unindent) In answer to your questions and comments:

  • The presence of selective agonists and antagonists doesn't mean their should be a seperate page.

It doesn't preclude it either.

  • There are vaguely selective agonists for a huge number of subtype combinations; of which in total there are over 10,000.

As mentioned here, very selective agonists and antagonists for the GABAA-ρ receptor subclass have been identified. While the theoretical number of GABAA receptors as you point out is astronomical, the number of documented receptor subtypes is much smaller (a few dozen at most).

  • GABAA-ρ receptor? ρ what? 1 2 or 3? All receptors containg ρ subunits?

As discussed here, the answer is very straight forward: all homo- or hetero-pentamers where each monomer is selected from the group ρ1, ρ2, and/or ρ3.

  • not all receptors with ρ subunits are GABAC receptors

Are you referring to ρ1γ2 receptors (see references here)? However this point becomes moot since my proposal was to rename the "GABAC" article to "GABAA-ρ"

  • if you have a page for GABAA-ρ receptor you need to have one for GABAA-alpha receptor GABAA-beta receptors

There is strong evidence for functional rho homo- and hetero-pentamers (ρ15, ρ25, ρ35, ρ1mρ2n, ρ2mρ3n) while there is no evidence for the corresponding alpha or beta homo-pentamers. Hence there is strong justification for a separate rho article but much less justification for separate alpha or beta subfamily articles.

  • ρ homomers are unusual, but so are delta containing GABAA receptors, alpha4 and alpha6 containing GABAA receptors. alphabeta pentamers are interesting.

Again, the point is that the GABAA-ρ subclass is "self-contained" in the sense that functional receptors can be constructed solely from rho subunits. The same cannot be said of alpha, beta, or delta subunits.

  • But we don't have pages for them. We have pages for the subunit.

What might make sense is to have pages for confirmed functional oligomers (similar to some of the nicotinic acetylcholine receptors such as (α4)2(β2)3).

  • If you then say we need a page for every CONFIRMED receptor, then we still don't have a page on ρ receptors, because we don't know what the ρ homomers are made of? (ρ1)2(ρ2)2(ρ3)? We have no idea.

As discussed here, there is in fact published data which sheds light on the specific subunit composition of functional rho pentamers. Boghog2 (talk) 05:41, 15 May 2009 (UTC)


Just because there are 10,000 possible combinations of GABAA subunits doesn't mean they are all notable, but the ones that are notable should have their own page. There are also ligands available which are selective for GABAA receptors containing α5 subunits, and these are listed on the α5 subunit page for convenience, as presumably there are a whole range of GABAA pentamers which can contain an α5 subunit. However even if the "GABAC" receptor is actually a GABAA-ρ pentamer then it still makes sense for it to have its own page as it is a particular subunit combination which is notable in its own right due to having defined pharmacology and selective ligands. See for comparison the Alpha-7 nicotinic receptor which again is notable enough to have its own page, whereas there is as yet no page for the (nicotinic) α1β1δε pentamer (but eventually there probably will be). Probably would be better to rename the GABAC receptor page to GABAA-ρ, although as Boghog2 points out there are still articles published in 2009 that use the old terminology, so it is perhaps premature to say it has been entirely superseded like the 5-HT1C has been. Meodipt (talk) 00:48, 16 May 2009 (UTC)
Thanks for your comments. I have renamed the GABAC receptor page to GABAA-ρ while mentioning that GABAC was the previous name in the lead. Hopefully this is a reasonable compromise that everyone will accept. Boghog2 (talk) 09:33, 16 May 2009 (UTC)

I still think this is not an optimum way to look at it. It seems we can agree that the availability of selective agonists is irrelevant to whether or not a receptor of a particular subtype make up deserves in own page. As you say, only a few receptors of an exact subtype have been document, but rho containing receptors are not one of them; we have some idea, but it is far from certain. While I don't think having a page for every confirmed subtype is a particularly bad option, I think it not the best way. Why have a page on alpha1beta2gamma2 and another on alpha1beta3gamma2? The two receptors are almost identical. But it seems that your leading point is that rho receptors are "self contained". They can be, but as I've said, there is substantial evidence, even in the retina, that rho receptors form with gamma and alpha1 subunits.

To me, it seems that our biggest problem here is lack of knowledge. If we knew that in naitive tissue, say, rho1 homomers were actually responsible for 99% of GABAC type pharmacology, then I don't think we would be having this debate.

As I've said, I think the optimum solution is for discuss alpha1 containing receptors on the page for the alpha1 subunit, rho1 containing receptors in the rho1 page. Right now 99% of these subunit pages are super stuby, and this would give them some purspose. Moreover, it still strikes me that GABAA-ρ is just being used as a byword for GABAC receptors, by putting the evidence on rho1 homomers as well as rho1alpha1gamma2 on the rho page you would avoid this.

The problem with this way is redundancy, but we already have plenty of this, and, at least to me, this way organizes the redundancy in a meaninful way, i.e. instead of having a page on GABAA receptors, GABAA-ρ receptors, ρ1 subunit, and (ρ1)5 receptors; you have a page on GABAA receptors and ρ1 subunits.

But I dear say you disagree, and if you do, I shant push the matter any further Bilz0r (talk) 22:43, 17 May 2009 (UTC)

You raise some good points, but as you say there is a lack of knowledge about the rho-containing GABAA receptors and I think the current arrangement works for now (especially as there is still research being published in 2009 using the old terminology). Once there is more information available about the function and makeup of ρ1 homomers and other rho-containing receptors then by all means change it to reflect the state of knowledge at that time. As an aside though I don't see anything wrong with having seperate pages for GABAA receptors, GABAA-ρ receptors, ρ1 subunit, and (ρ1)5 receptors seeing as they are all subtly distinct topics, and can still be easily linked together where needed. Meodipt (talk) 23:03, 17 May 2009 (UTC)

More GABAC ranting

Okay, forgetting about how your going to set up other pages, the sentence is misleading: "Three general classes of GABA receptor are known: GABAA and GABAA-ρ (formerly designated GABAС) ionotropic receptors," There are two clases, GABAA, and GABAB. If you want to discuess how rho containing receptors differ from other members of the GABAA receptor family, fine; do it on as many pages as you feel is necessay. But you can't say GABAA and GABAA-rho are different classes, one is, without question, a subset of the other. Bilz0r (talk) 21:19, 18 May 2009 (UTC)

Fixed with this edit. Boghog2 (talk) 22:35, 18 May 2009 (UTC)

GABA in insects

Regarding the line: "In insect species GABA acts only on excitatory nerve receptors."

This seems strange to me. Is there any citation supporting this claim? Maybe it should read In "certain insect species". Then, which ones?


This article is about excitatory actions of GABA in cockroaches:

http://jeb.biologists.org/cgi/content/abstract/212/1/126

Here, we find information about inhibitory GABA effects in honeybees:

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WNM-4TF07TW-1&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&_docanchor=&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=6f5eb3698d45e4af68852301c9589c15 —Preceding unsigned comment added by 91.23.175.74 (talk) 21:46, 11 July 2009 (UTC)

Much more needed on health effects +&-, drugs affecting

GABA agonists

Topamax (Topiramate)

Neurontin (Gabapentin)

Help treat migraine, have side effects possibly including arrhythmias, tachycardia

GABA may calm elder adult brain, allowing better focus executive function.

Excess GABA may interfere with working memory in elderly adults.

GABA may be enhanced by Red Rice Yeast, Lovastatin. Additive effects. (maybe part of its anti-inflammatory function).

GABA may be a "hypotensive agent" —Preceding unsigned comment added by 66.167.95.208 (talk) 20:29, 12 December 2010 (UTC)

Effectiveness of GABA health drinks?

If GABA doesn't cross the blood-brain barrier, does this mean that the Jones Soda Co.'s GABA-laced health drink, which claims to promote "focus + clarity", doesn't actually do anything? —Robotech_Master (talk) 14:50, 26 May 2011 (UTC)

It's just deceitful marketing hype. Deli nk (talk) 15:12, 26 May 2011 (UTC)
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