Talk:Gamma-aminobutyric acid

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[edit] 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

[edit] 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)

[edit] 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.

[edit] 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)

[edit] 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)

[edit] 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)

[edit] 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[2] 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)

[edit] 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))

[edit] 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)

[edit] 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)

[edit] 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)

[edit] "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)