View source for Gamma-Aminobutyric acid

{{Redirect|GABA}}
{{DISPLAYTITLE:''gamma''-Aminobutyric acid}}
{{chembox
| verifiedrevid = 310851955
|  Name=''gamma''-Aminobutyric acid
|  ImageFile = Gamma-Aminobuttersäure - gamma-aminobutyric acid.svg
|  ImageSize = 230
|  ImageName = Simplified structural formula
|  ImageFile1 = GABA-3D-balls.png
|  ImageSize1 = 230
|  ImageName1 = Ball-and-stick model
|  IUPACName = 4-aminobutanoic acid
|  OtherNames=
|Section1= {{Chembox Identifiers
|  CASNo_Ref = {{cascite}}
| CASNo=56-12-2
|  PubChem=119
| IUPHAR_ligand = 1067
|  ChemSpiderID = 116
|  SMILES=C(CC(=O)O)CN
|  MeSHName=gamma-Aminobutyric+Acid
  }}
|Section2= {{Chembox Properties
|  Formula=C<sub>4</sub>H<sub>9</sub>NO<sub>2</sub>
|  MolarMass=103.12 g/mol
|  Appearance=
|  Density=
|  MeltingPtC=203.7
|  BoilingPt=
|  Solubility=
  }}
|Section3= {{Chembox Hazards
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'''γ-Aminobutyric acid''' ('''GABA''') ({{pron-en|ˈɡæmə əˈmiːnoʊbjuːˈtɪrɨk ˈæsɨd}}, or the acronym {{IPA-en|ˈɡæbə|}}) is the chief inhibitory [[neurotransmitter]] in the [[mammal]]ian [[central nervous system]]. It plays a role in regulating [[neuron]]al excitability throughout the [[nervous system]]. In humans, GABA is also directly responsible for the regulation of [[muscle tone]].<ref name="pmid11837891">{{cite journal | author = Watanabe M, Maemura K, Kanbara K, Tamayama T, Hayasaki H | title = GABA and GABA receptors in the central nervous system and other organs | journal = Int. Rev. Cytol. | volume = 213 | issue = | pages = 1–47 | year = 2002 | pmid = 11837891 | doi = 10.1016/S0074-7696(02)13011-7| url = | issn = }}</ref> In [[insect]] species GABA acts only on excitatory nerve receptors.

Although chemically it is an [[amino acid]], GABA is rarely referred to as such in the scientific or medical communities, because the term "amino acid," used without a [[qualifier]], refers to the [[alpha amino acid]]s, which GABA is not, nor is it incorporated into [[protein]]s.

In [[spastic diplegia]] in humans, GABA absorption becomes impaired by nerves damaged from the condition's [[upper motor neuron]] lesion, which leads to [[hypertonia]] of the muscles signaled by those nerves that can no longer absorb GABA.

== Function ==
=== Neurotransmitter ===

In [[vertebrates]], GABA acts at inhibitory [[chemical synapse|synapses]] in the [[brain]] by binding to specific transmembrane [[Receptor (biochemistry)|receptor]]s in the [[plasma membrane]] of both pre- and postsynaptic neuronal processes.  This binding causes the opening of [[ion channel]]s to allow the flow of either negatively charged [[chloride]] ions into the [[cell (biology)|cell]] or positively charged [[potassium]] ions out of the cell. Depending on which ion channels open, the membrane potential is either hyperpolarized or depolarized. This action results in a negative change in the [[transmembrane potential]], usually causing [[hyperpolarization (biology)|hyperpolarization]]. Two general classes of [[GABA receptor]] are known: [[GABAA receptor|GABA<sub>A</sub>]] in which the receptor is part of a [[ligand-gated ion channel]] complex, and [[GABAB receptor|GABA<sub>B</sub>]] [[metabotropic receptor]]s, which are [[G protein-coupled receptor]]s that open or close ion channels via intermediaries ([[G protein]]s).

[[Image:GABAergic-synapse.gif|left|thumb|500px|The production, release, action and degradation of GABA at a stereotyped GABAergic synapse]]Neurons that produce GABA as their output are called GABAergic neurons, and have chiefly inhibitory action at receptors in the adult vertebrate.  [[Medium spiny neuron|Medium Spiny Cells]] are a typical example of inhibitory [[Central nervous system|CNS]] GABAergic cells. In contrast, GABA exhibits excitatory actions in [[insect]]s, mediating [[muscle]] activation at synapses between [[nerve]]s and muscle cells, and also the stimulation of certain [[gland]]s. In mammals, some GABAergic neurons, such as [[chandelier cell]]s, are also able to excite their glutamatergic counterparts.<!--

--><ref name="pmid16410524">{{cite journal | author = Szabadics J, Varga C, Molnár G, Oláh S, Barzó P, Tamás G | title = Excitatory effect of GABAergic axo-axonic cells in cortical microcircuits | journal = Science | volume = 311 | issue = 5758 | pages = 233–5 | year = 2006 | month = January | pmid = 16410524 | doi = 10.1126/science.1121325 | url = }}</ref>

[[GABAA receptor|GABA<sub>A</sub> receptors]] are chloride channels; that is, when activated by GABA, they allow the flow of [[chloride]] ions across the membrane of the cell. Whether this chloride flow is excitatory/depolarizing (makes the voltage across the cell's membrane less negative), shunting (has no effect on the cell's membrane) or inhibitory/hyperpolarizing (makes the cell's membrane more negative) depends on the direction of the flow of chloride. When net chloride flows out of the cell, GABA is excitatory or depolarizing; when the net chloride flows into the cell, GABA is inhibitory or hyperpolarizing. When the net flow of chloride is close to zero, the action of GABA is shunting. [[Shunting inhibition]] has no direct effect on the membrane potential of the cell, however it minimises the effect of any coincident synaptic input essentially by reducing the electrical resistance of the cell's membrane (essentially equivalent to [[Ohm's law]]). A developmental switch in the molecular machinery controlling concentration of chloride inside the cell and hence the direction of this ion flow, is responsible for the changes in the functional role of GABA between the [[neonatal]] and adult stages. That is to say, GABA's role changes from excitatory to inhibitory as the brain develops into adulthood.<ref name="pmid18500393">{{cite journal | author = Li K, Xu E | title = The role and the mechanism of gamma-aminobutyric acid during central nervous system development | journal = Neurosci Bull | volume = 24 | issue = 3 | pages = 195–200 | year = 2008 | month = June | pmid = 18500393 | doi = 10.1007/s12264-008-0109-3| url = | issn = }}</ref>

=== Development ===
In [[hippocampus]] and [[neocortex]] of the mammalian brain, GABA has primarily excitatory effects early in development, and is in fact the major excitatory neurotransmitter in many regions of the brain before the maturation of glutamate synapses - ''See'' [[Neural development|''developing cortex'']].<ref name="pmid18500393"/>

In the developmental stages preceding the formation of synaptic contacts, GABA is synthesized by neurons and acts both as an [[autocrine]] (acting on the same cell) and [[paracrine]] (acting on nearby cells) signalling mediator.<ref name="isbn0-87893-697-1">{{cite book | author = Purves D, Fitzpatrick D, Hall WC, Augustine GJ, Lamantia A-S | authorlink = | editor = | others = | title = Neuroscience | edition = 4th | language = | publisher = Sinauer | location = Sunderland, Mass | year = 2007 | origyear = | pages = 135, box 6D |quote = | isbn = 0-87893-697-1 | oclc = | doi = | url = | accessdate = }}</ref><ref name="pmid16512345">{{cite journal | author = Jelitai M, Madarasz E | title = The role of GABA in the early neuronal development | journal = Int. Rev. Neurobiol. | volume = 71 | issue = | pages = 27–62 | year = 2005 | pmid = 16512345 | doi = 10.1016/S0074-7742(05)71002-3| url = http://www.iem.cas.cz/Data/files/pdf/neuroscience/2004/jelitai-2004.pdf | format = {{dead link|date=October 2009}} }}</ref>

GABA regulates the proliferation of neural [[progenitor cell]]s<ref name="pmid8845153">{{cite journal | author = LoTurco JJ, Owens DF, Heath MJ, Davis MB, Kriegstein AR | title = GABA and glutamate depolarize cortical progenitor cells and inhibit DNA synthesis | journal = Neuron | volume = 15 | issue = 6 | pages = 1287–98 | year = 1995 | month = December | pmid = 8845153 | doi = 10.1016/0896-6273(95)90008-X| url = }}</ref><ref name="pmid10908617">{{cite journal | author = Haydar TF, Wang F, Schwartz ML, Rakic P | title = Differential modulation of proliferation in the neocortical ventricular and subventricular zones | journal = J. Neurosci. | volume = 20 | issue = 15 | pages = 5764–74 | year = 2000 | month = August | pmid = 10908617 | doi = | url = http://www.jneurosci.org/cgi/pmidlookup?view=long&pmid=10908617 | issn = }}</ref> the migration<ref name="pmid9698329">{{cite journal | author = Behar TN, Schaffner AE, Scott CA, O'Connell C, Barker JL | title = Differential response of cortical plate and ventricular zone cells to GABA as a migration stimulus | journal = J. Neurosci. | volume = 18 | issue = 16 | pages = 6378–87 | year = 1998 | month = August | pmid = 9698329 | doi = | url = http://www.jneurosci.org/cgi/pmidlookup?view=long&pmid=9698329 | issn = }}</ref> and [[cellular differentiation|differentiation]]<ref name="pmid8390627">{{cite journal | author = Barbin G, Pollard H, Gaïarsa JL, Ben-Ari Y | title = Involvement of GABAA receptors in the outgrowth of cultured hippocampal neurons | journal = Neurosci. Lett. | volume = 152 | issue = 1-2 | pages = 150–4 | year = 1993 | month = April | pmid = 8390627 | doi = 10.1016/0304-3940(93)90505-F| url =  }}</ref><ref name="pmid11371348">{{cite journal | author = Ganguly K, Schinder AF, Wong ST, Poo M | title = GABA itself promotes the developmental switch of neuronal GABAergic responses from excitation to inhibition | journal = Cell | volume = 105 | issue = 4 | pages = 521–32 | year = 2001 | month = May | pmid = 11371348 | doi = 10.1016/S0092-8674(01)00341-5| url = }}</ref> the elongation of [[neurite]]s<ref name="pmid11264309">{{cite journal | author = Maric D, Liu QY, Maric I, Chaudry S, Chang YH, Smith SV, Sieghart W, Fritschy JM, Barker JL | title = GABA expression dominates neuronal lineage progression in the embryonic rat neocortex and facilitates neurite outgrowth via GABA(A) autoreceptor/Cl- channels | journal = J. Neurosci. | volume = 21 | issue = 7 | pages = 2343–60 | year = 2001 | month = April | pmid = 11264309 | doi = | url = http://www.jneurosci.org/cgi/pmidlookup?view=long&pmid=11264309 | issn = }}</ref> and the  formation of synapses.<ref name="pmid12209121">{{cite journal | author = Ben-Ari Y | title = Excitatory actions of gaba during development: the nature of the nurture | journal = Nat. Rev. Neurosci. | volume = 3 | issue = 9 | pages = 728–39 | year = 2002 | month = September | pmid = 12209121 | doi = 10.1038/nrn920 | url =  }}</ref>

GABA also regulates the growth of [[embryonic stem cell|embryonic]] and [[neural stem cell]]s. GABA can inﬂuence the development of neural progenitor cells via [[brain-derived neurotrophic factor]] (BDNF) expression.<ref name="pmid12163549">{{cite journal | author = Obrietan K, Gao XB, Van Den Pol AN | title = Excitatory actions of GABA increase BDNF expression via a MAPK-CREB-dependent mechanism--a positive feedback circuit in developing neurons | journal = J. Neurophysiol. | volume = 88 | issue = 2 | pages = 1005–15 | year = 2002 | month = August | pmid = 12163549 | doi = | url = http://jn.physiology.org/cgi/pmidlookup?view=long&pmid=12163549 | issn = }}</ref> GABA activates the [[GABAA receptor|GABA<sub>A</sub> receptor]], causing cell cycle arrest in the S-phase, limiting growth.<ref>{{cite journal |author=Wang DD, Kriegstein AR, Ben-Ari Y |title=GABA Regulates Stem Cell Proliferation before Nervous System Formation |journal=Epilepsy currents / American Epilepsy Society |volume=8 |issue=5 |pages=137–9 |year=2008 |pmid=18852839 |pmc=2566617 |doi=10.1111/j.1535-7511.2008.00270.x}}</ref>

===Beyond the nervous system===
[[File:PMID19190758 PLoS 0004371.png|thumb|240px|GABA-producing [[GAD67]] enzyme in the brain slice at 1st postnatal day, with the highest expression in [[subventricular zone]] (svz). From Popp et al., 2009.<ref name="pmid19190758">{{cite journal |author=Popp A, Urbach A, Witte OW, Frahm C |title=Adult and embryonic GAD transcripts are spatiotemporally regulated during postnatal development in the rat brain |journal=[[PLoS ONE]] |volume=4 |issue=2 |pages=e4371 |year=2009 |pmid=19190758 |pmc=2629816|doi=10.1371/journal.pone.0004371 |url=http://dx.plos.org/10.1371/journal.pone.0004371}}</ref>]]GABAergic mechanisms have been demonstrated in various peripheral tissues and organs including, but not restricted to the intestine, stomach, pancreas, Fallopian tube, uterus, ovary, testis, kidney, urinary bladder, lung and liver.<ref>{{cite journal |author=Erdö SL, Wolff JR |title=gamma-Aminobutyric acid outside the mammalian brain |journal=J. Neurochem. |volume=54 |pages=363–72 |year=1990 |pmid=2405103 |doi=10.1111/j.1471-4159.1990.tb01882.x |issue=2}}</ref>
 
In 2007, an excitatory GABAergic system was described in the airway [[epithelium]]. The system activates following exposure to allergens and may participate in the mechanisms of [[asthma]].<ref name="GABA_lungs">{{cite pmid|17589520}}</ref>  GABAergic systems have also been found in the [[testis]]<ref name="Inyerballs">{{cite book|last=Payne|first=Anita H.|coauthors=Matthew H. Hardy|title=The Leydig cell in health and disease|publisher=Humana Press|year=2007|isbn=1588297543, ISBN 9781588297549}}</ref> and in the eye lens.<ref name="GABA_lens">{{cite pmid|17969168}}</ref>

== Structure and conformation ==

GABA is found mostly as a [[zwitterion]], that is, with the [[carboxy]] group deprotonated and the amino group protonated. Its [[conformational isomerism|conformation]] depends on its environment. In the gas phase, a highly folded conformation is strongly favored because of the electrostatic attraction between the two functional groups. The stabilization is about 50 kcal/mol, according to [[quantum chemistry]] calculations. In the solid state, a more extended conformation is found, with a trans conformation at the amino end and a gauche conformation at the carboxyl end. This is due to the packing interactions with the neighboring molecules. In solution, five different conformations, some folded and some extended are found as a result of [[solvation]] effects. The conformational flexibility of GABA is important for its biological function, as it has been found to bind to different receptors with different conformations. Many GABA analogues with pharmaceutical applications have more rigid structures in order to control the binding better.<ref>Devashis Majumdar and Sephali Guha.(1988). "Conformation, electrostatic potential and pharmacophoric pattern of GABA (gamma-aminobutyric acid) and several GABA inhibitors." ''Journal of Molecular Structure: THEOCHEM''  '''180''': 125-140. {{doi|10.1016/0166-1280(88)80084-8}}</ref><ref>Anne-Marie Sapse. ''Molecular Orbital Calculations for Amino Acids and Peptides''. Birkhäuser, '''2000'''. ISBN 0817638938.</ref>

== History ==

Gamma-aminobutyric acid was first synthesized in 1883,{{Citation needed|date=August 2009}} and was first known only as a plant and microbe metabolic product. In 1950, however, GABA was discovered to be an integral part of the mammalian [[central nervous system]].<ref name="isbn0-19-514008-7">{{cite book | author = Roth, Robert J.; Cooper, Jack R.; Bloom, Floyd E. | title = The Biochemical Basis of Neuropharmacology | publisher = Oxford University Press | location = Oxford [Oxfordshire] | year = 2003 | pages = 416 pages | isbn = 0-19-514008-7 | oclc = | doi = }}</ref>

== Synthesis ==

Since GABA doesn't penetrate the blood brain barrier, GABA is  therefore synthesized in vivo. It's synthesized from [[glutamate]] using the [[enzyme]] [[L-glutamic acid decarboxylase]] and [[pyridoxal phosphate]] (which is the active form of vitamin B6) as a [[cofactor (biochemistry)|cofactor]] via a metabolic pathway called the GABA shunt. This process converts glutamate, the principal [[excitation|excitatory]] neurotransmitter, into the principal inhibitory neurotransmitter (GABA).<ref name="pmid12467378">{{cite journal | author = Petroff OA | title = GABA and glutamate in the human brain | journal = Neuroscientist | volume = 8 | issue = 6 | pages = 562–73 | year = 2002 | month = December | pmid = 12467378 | doi = 10.1177/1073858402238515| url = http://nro.sagepub.com/cgi/pmidlookup?view=long&pmid=12467378 | issn = }}</ref><ref name="pmid17499106">{{cite journal | author = Schousboe A, Waagepetersen HS | title = GABA: homeostatic and pharmacological aspects | journal = Prog. Brain Res. | volume = 160 | issue = | pages = 9–19 | year = 2007 | pmid = 17499106 | doi = 10.1016/S0079-6123(06)60002-2 | url = | issn = }}</ref>

== Pharmacology ==

Drugs that act as [[agonist]]s of [[GABA receptor]]s (known as GABA analogues or ''GABAergic'' drugs) or increase the available amount of GABA typically have relaxing, anti-anxiety and anti-convulsive effects.<ref name="pmid16377242">{{cite journal | author = Foster AC, Kemp JA | title = Glutamate- and GABA-based CNS therapeutics | journal = Curr Opin Pharmacol | volume = 6 | issue = 1 | pages = 7–17 | year = 2006 | month = February | pmid = 16377242 | doi = 10.1016/j.coph.2005.11.005 | url = | issn = }}</ref>,<ref>[[:fr:Georges Chapouthier|Chapouthier, G]], Venault P., A pharmacological link between epilepsy and anxiety ?, Trends in Pharmacological Sciences, 2001, 22(10), 491-493}}</ref>. Many of the substances below are known to cause [[anterograde amnesia]] and [[retrograde amnesia]].

In general, GABA does not cross the [[blood-brain barrier]],<ref>{{cite journal |author=Kuriyama K, Sze PY |title=Blood-brain barrier to H3-gamma-aminobutyric acid in normal and amino oxyacetic acid-treated animals |journal=Neuropharmacology |volume=10 |issue=1 |pages=103–8 |year=1971 |month=January |pmid=5569303 |doi= 10.1016/0028-3908(71)90013-X|url=}}</ref> although certain areas of the brain which have no effective blood brain barrier, such as the [[periventricular nucleus]], can be reached by drugs such as systematically injected GABA.<ref name=Muller1999/> At least one study suggests that orally administered GABA increases the amount of [[Human Growth Hormone]].<ref name=Powers2008>{{cite journal | author = Powers ME, Yarrow JF, McCoy SC, Borst SE | title = Growth hormone isoform responses to GABA ingestion at rest and after exercise | journal = Medicine and science in sports and exercise | volume = 40 | issue = 1 | pages = 104–10 | year = 2008 | month = January | pmid = 18091016 | doi = 10.1249/mss.0b013e318158b518| url = http://www.ncbi.nlm.nih.gov/pubmed/18091016 | issn = 1530-031}}</ref> GABA directly injected to the brain has been reported to have both stimulatory and inhibitory effects on the production of growth hormone, depending on the physiology of the individual.<ref name=Muller1999>{{cite journal |author=Müller EE, Locatelli V, Cocchi D |title=Neuroendocrine control of growth hormone secretion |journal=Physiol. Rev. |volume=79 |issue=2 |pages=511–607 |year=1999 |month=April |pmid=10221989 |doi= |url=}} [http://physrev.physiology.org/cgi/content/full/79/2/511 Free full-text].</ref>

== GABAergic Drugs ==

* GABA<sub>A</sub> receptor ligands
** Agonists/Positive allosteric modulators: [[ethanol|alcohol]]<ref name="pmid12692303">{{cite journal | author = Dzitoyeva S, Dimitrijevic N, Manev H | title = Gamma-aminobutyric acid B receptor 1 mediates behavior-impairing actions of alcohol in Drosophila: adult RNA interference and pharmacological evidence | journal = Proc. Natl. Acad. Sci. U.S.A. | volume = 100 | issue = 9 | pages = 5485–90 | year = 2003 | pmid = 12692303 | doi = 10.1073/pnas.0830111100 | pmc = 154371 }}</ref><ref name="pmid9311780">{{cite journal | author = Mihic SJ, Ye Q, Wick MJ, Koltchine VV, Krasowski MD, Finn SE, Mascia MP, Valenzuela CF, Hanson KK, Greenblatt EP, Harris RA, Harrison NL | title = Sites of alcohol and volatile anaesthetic action on GABA<sub>A</sub> and glycine receptors | journal = Nature | volume = 389 | issue = 6649 | pages = 385–9 | year = 1997 | pmid = 9311780 | doi = 10.1038/38738}}</ref><ref name="pmid17175815">{{cite journal | author = Boehm SL, Ponomarev I, Blednov YA, Harris RA | title = From gene to behavior and back again: new perspectives on GABA<sub>A</sub>receptor subunit selectivity of alcohol actions | journal = Adv. Pharmacol. | volume = 54 | issue = | pages = 171–203 | year = 2006 | pmid = 17175815 | doi = 10.1016/j.bcp.2004.07.023}}</ref>, [[barbiturate]]s, [[benzodiazepine]]s, [[carisoprodol]], [[etomidate]], [[glutethimide]], [[L-theanine]], [[kava]], [[methaqualone]], [[muscimol]], [[neuroactive steroid]]s, [[nonbenzodiazepine]]s, [[propofol]], [[Scutellaria lateriflora|scullcap]], [[Valerian (herb)|valerian]], [[Volatile anaesthetic|volatile]]/[[Inhalational anaesthetic|inhaled anaesthetic]]s.
** Antagonists/Negative allosteric modulators: [[bicuculline]], [[cicutoxin]], [[flumazenil]], [[furosemide]], [[gabazine]], [[oenanthotoxin]], [[picrotoxin]], [[Ro15-4513]], [[thujone]].
* GABA<sub>B</sub> Receptor Ligands
** Agonists: [[baclofen]], [[gamma-Butyrolactone|GBL]], [[gamma-Hydroxybutyric acid|GHB]]<ref name="pmid16129424">{{cite journal | author = Dimitrijevic N, Dzitoyeva S, Satta R, Imbesi M, Yildiz S, Manev H | title = Drosophila GABA<sub>B</sub> receptors are involved in behavioral effects of gamma-hydroxybutyric acid (GHB) | journal = Eur. J. Pharmacol. | volume = 519 | issue = 3 | pages = 246–52 | year = 2005 | pmid = 16129424 | doi = 10.1016/j.ejphar.2005.07.016 }}</ref>, [[phenibut]].
** Antagonists: [[phaclofen]], [[saclofen]].
* [[GABA reuptake inhibitor]]s: [[deramciclane]], [[hyperforin]], [[tiagabine]].
* GABA-transaminase inhibitors: [[gabaculine]], [[phenelzine]], [[valproate]], [[vigabatrin]], [[Lemon balm]] (Melissa officinalis) <ref>{{cite web | title=Bioassay-guided fractionation of lemon balm (Melissa officinalis L.) using an in vitro measure of GABA transaminase activity | url=http://www.ncbi.nlm.nih.gov/pubmed/19165747 | accessdate=2010-03-08}}</ref>.
* GABA analogues: [[pregabalin]], [[gabapentin]].
* Others: GABA (itself), [[L-glutamine]], [[picamilon]], [[progabide]], [[tetanospasmin]].

== See also ==

* [[Spasticity]]
* [[Spastic diplegia]], a GABA deficiency [[neuromuscular]] [[neuropathology]]

== References ==
{{Reflist|2}}

== External links ==
* {{cite web | url = http://www.vcu-cme.org/gaba/overview.html | title =  GABA | author = Lydiard B, Pollack MH, Ketter TA, Kisch E, Hettema JM | authorlink = | coauthors = | date = 2001-10-26 | work = Continuing Medical Education | publisher = School of Medicine, Virginia Commonwealth University, Medical College of Virginia Campus (VCU), Richmond, VA  | pages = | language = | archiveurl = | archivedate = | quote =  The role of GABA in the pathogenesis and treatment of anxiety and other neuropsychiatric disorders | accessdate = 2008-06-20}}
* [http://www.scholarpedia.org/article/Gamma-aminobutyric_acid Scholarpedia article on GABA]

{{GABAergics}}
{{GABAAergics}}
{{Neurotransmitters}}

{{DEFAULTSORT:Aminobutyric Acid, Gamma-}}
[[Category:Anticonvulsants]]
[[Category:Neurotransmitters]]
[[Category:Amino acids]]
[[Category:GABA analogues|*]]

[[ca:Àcid γ-aminobutíric]]
[[cs:Kyselina gama-aminomáselná]]
[[da:GABA]]
[[de:Γ-Aminobuttersäure]]
[[et:Γ-aminovõihape]]
[[es:Ácido γ-aminobutírico]]
[[eo:Gamo-Aminobuteracido]]
[[fr:Acide γ-aminobutyrique]]
[[ko:감마 아미노낙산]]
[[id:Asam gamma-aminobutirat]]
[[it:Acido γ-amminobutirrico]]
[[he:GABA]]
[[hu:Gamma-amino-vajsav]]
[[nl:Gamma-aminoboterzuur]]
[[ja:Γ-アミノ酪酸]]
[[no:GABA]]
[[pl:Kwas γ-aminomasłowy]]
[[pt:Ácido gama-aminobutírico]]
[[ru:Гамма-аминомасляная кислота]]
[[simple:Gamma-Aminobutyric acid]]
[[sk:Kyselina gama-aminomaslová]]
[[sl:Γ-aminomaslena kislina]]
[[fi:Gamma-aminovoihappo]]
[[sv:GABA]]
[[ta:காமா அமினோ புயூட்டைரிக் காடி]]
[[tr:Gamma aminobütirik asit]]
[[uk:Гамма-аміномасляна кислота]]
[[zh:Γ-氨基丁酸]]
[[Category:2Fix]]