Gamma - aminobutyric acid - wikipedia Gamma - aminobutyric acid `` GABA '' redirects here. For other uses, see GABA ( disambiguation ). This article has multiple issues. Please help improve it or discuss these issues on the talk page. ( Learn how and when to remove these template messages ) This article needs more medical references for verification or relies too heavily on primary sources. Please review the contents of the article and add the appropriate references if you can. Unsourced or poorly sourced material may be challenged and removed. ( June 2015 ) This article needs attention from an expert on the subject. Please add a reason or a talk parameter to this template to explain the issue with the article. When placing this tag, consider associating this request with a WikiProject. ( September 2016 ) gamma - Aminobutyric acid Names IUPAC name 4 - aminobutanoic acid Identifiers CAS Number 56 - 12 - 2 3D model ( JSmol ) Interactive image ChEBI CHEBI : 16865 ChemSpider 116 DrugBank DB02530 ECHA InfoCard 100.000. 235 EC Number 200 - 258 - 6 IUPHAR / BPS 1067 KEGG D00058 MeSH gamma - Aminobutyric + Acid PubChem CID 119 RTECS number ES6300000 UNII 2ACZ6IPC6I InChI InChI = 1S / C4H9NO2 / c5 - 3 - 1 - 2 - 4 ( 6 ) 7 / h1 - 3, 5H2, ( H, 6, 7 ) Key : BTCSSZJGUNDROE - UHFFFAOYSA - N InChI = 1 / C4H9NO2 / c5 - 3 - 1 - 2 - 4 ( 6 ) 7 / h1 - 3, 5H2, ( H, 6, 7 ) Key : BTCSSZJGUNDROE - UHFFFAOYAC SMILES C ( CC ( = O ) O ) CN Properties Chemical formula C H NO Molar mass 103.120 g / mol Appearance white microcrystalline powder Density 1.11 g / mL Melting point 203.7 ° C ( 398.7 ° F ; 476.8 K ) Boiling point 247.9 ° C ( 478.2 ° F ; 521.0 K ) Solubility in water 130 g / 100 mL log P − 3.17 Acidity ( pK ) 4.23 ( carboxyl ), 10.43 ( amino ) Hazards Main hazards Irritant, Harmful Lethal dose or concentration ( LD, LC ) : LD ( median dose ) 12,680 mg / kg ( mouse, oral ) Except where otherwise noted, data are given for materials in their standard state ( at 25 ° C ( 77 ° F ), 100 kPa ). N verify ( what is ? ) Infobox references gamma - Aminobutyric acid ( γ - Aminobutyric acid ) / ˈɡæmə əˈmiːnoʊbjuːˈtɪrɪk ˈæsɪd / ( GABA / ˈɡæbə / ) is the chief inhibitory neurotransmitter in the mammalian central nervous system. Its principal role is reducing neuronal excitability throughout the nervous system. In humans, GABA is also directly responsible for the regulation of muscle tone. Contents 1 Function 1.1 Neurotransmitter 1.2 Brain development 1.3 Beyond the nervous system 2 Structure and conformation 3 History 4 Biosynthesis 5 Catabolism 6 Pharmacology 7 Chemistry 8 GABAergic drugs 9 In plants 10 See also 11 References 12 Bibliography 13 External links Function Neurotransmitter GABA metabolism, involvement of glial cells In vertebrates, GABA acts at inhibitory synapses in the brain by binding to specific transmembrane receptors in the plasma membrane of both pre - and postsynaptic neuronal processes. This binding causes the opening of ion channels to allow the flow of either negatively charged chloride ions into the cell or positively charged potassium ions out of the cell. This action results in a negative change in the transmembrane potential, usually causing hyperpolarization. Two general classes of GABA receptor are known : GABA in which the receptor is part of a ligand - gated ion channel complex GABA metabotropic receptors, which are G protein - coupled receptors that open or close ion channels via intermediaries ( G proteins ) 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 cells are a typical example of inhibitory central nervous system GABAergic cells. In contrast, GABA exhibits both excitatory and inhibitory actions in insects, mediating muscle activation at synapses between nerves and muscle cells, and also the stimulation of certain glands. In mammals, some GABAergic neurons, such as chandelier cells, are also able to excite their glutamatergic counterparts. GABA receptors are ligand - activated chloride channels : when activated by GABA, they allow the flow of chloride ions across the membrane of the cell. Whether this chloride flow is depolarizing ( makes the voltage across the cell 's membrane less negative ), shunting ( has no effect on the cell 's membrane potential ), 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 depolarising ; when 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 reduces the effect of any coincident synaptic input by reducing the electrical resistance of the cell 's membrane. Shunting inhibition can `` override '' the excitatory effect of depolarising GABA, resulting in overall inhibition even if the membrane potential becomes less negative. It was thought that a developmental switch in the molecular machinery controlling concentration of chloride inside the cell changes the functional role of GABA between neonatal and adult stages. As the brain develops into adulthood, GABA 's role changes from excitatory to inhibitory. However, this theory of excitatory GABA in the developing brain has been questioned and subsequent studies in live neonatal rodents have directly shown GABA to be inhibitory in its action ( see next section ). Brain development While GABA is an inhibitory transmitter in the mature brain, its actions were thought to be primarily excitatory in the developing brain. The gradient of chloride was reported to be reversed in immature neurons, with its reversal potential higher than the resting membrane potential of the cell ; activation of a GABA - A receptor thus leads to efflux of Cl ions from the cell ( that is, a depolarizing current ). The differential gradient of chloride in immature neurons was shown to be primarily due to the higher concentration of NKCC1 co-transporters relative to KCC2 co-transporters in immature cells. GABA itself is partially responsible for orchestrating the maturation of ion pumps. GABAergic interneurons mature faster in the hippocampus and the GABA signalling machinery appears earlier than glutamatergic transmission. Thus, GABA was considered the major excitatory neurotransmitter in many regions of the brain before the maturation of glutamatergic synapses. However, this theory has been questioned based on results showing that in brain slices of immature mice incubated in artificial cerebrospinal fluid ( ACSF ) ( modified in a way that takes into account the normal composition of the neuronal milieu in sucklings by adding an energy substrate alternative to glucose, beta - hydroxybutyrate ) GABA action shifts from excitatory to inhibitory mode. This effect has been later repeated when other energy substrates, pyruvate and lactate, supplemented glucose in the slices ' media. Later investigations of pyruvate and lactate metabolism found that the original results were not due to energy source issues but to changes in pH resulting from the substrates acting as `` weak acids ''. These arguments were later rebutted by further findings showing that changes in pH even greater than that caused by energy substrates do not affect the GABA - shift described in the presence of energy substrate - fortified ACSF and that the mode of action of beta - hydroxybutyrate, pyruvate and lactate ( assessed by measurement NAD ( P ) H and oxygen utilization ) was energy metabolism - related. The true nature GABA effect in the developing brain has remained elusive until 2015, when the first study to directly show GABA action in live rodent brain has reported GABA to not be excitatory in its effect even though it slightly depolarised some neurons, confirming the dominance of shunting inhibition. In 2016, another study in live developing brains using optogenetics have shown GABA to be inhibitory, with GABAergic synapse activation leading to a reduction of network activity. That study has also shown that the same technique when used in brain slices instead records excitatory GABA effects, confirming the fact that excitatory GABA is most likely an artefact of in - vitro slice recordings. 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. The ganglionic eminences also contribute greatly to building up the GABAergic cortical cell population. GABA regulates the proliferation of neural progenitor cells the migration and differentiation the elongation of neurites and the formation of synapses. GABA also regulates the growth of embryonic and neural stem cells. GABA can influence the development of neural progenitor cells via brain - derived neurotrophic factor ( BDNF ) expression. GABA activates the GABA receptor, causing cell cycle arrest in the S - phase, limiting growth. Beyond the nervous system mRNA expression of the embryonic variant of the GABA - producing enzyme GAD67 in a coronal brain section of a one - day - old Wistar rat, with the highest expression in subventricular zone ( svz ) Besides the nervous system, GABA is also produced at relatively high levels in the insulin - producing β - cells of the pancreas. The β - cells secrete GABA along with insulin and the GABA binds to GABA receptors on the neighboring islet α - cells and inhibits them from secreting glucagon ( which would counteract insulin 's effects ). GABA can promote the replication and survival of β - cells and also promote the conversion of α - cells to β - cells, which may lead to new treatments for diabetes. GABA has also been detected in other peripheral tissues including intestines, stomach, Fallopian tubes, uterus, ovaries, testes, kidneys, urinary bladder, the lungs and liver, albeit at much lower levels than in neurons or β - cells. GABAergic mechanisms have been demonstrated in various peripheral tissues and organs, which include the intestines, the stomach, the pancreas, the Fallopian tubes, the uterus, the ovaries, the testes, the kidneys, the urinary bladder, the lungs, and the liver. Immune cells express receptors for GABA and administration of GABA can suppress inflammatory immune responses and promote `` regulatory '' immune responses, such that GABA administration has been shown to inhibit autoimmune diseases in several animal models. In 2007, an excitatory GABAergic system was described in the airway epithelium. The system is activated by exposure to allergens and may participate in the mechanisms of asthma. GABAergic systems have also been found in the testis and in the eye lens. GABA occurs in plants. Structure and conformation GABA is found mostly as a zwitterion ( i.e. with the carboxyl group deprotonated and the amino group protonated ). Its conformation depends on its environment. In the gas phase, a highly folded conformation is strongly favored due to the electrostatic attraction between the two functional groups. The stabilization is about 50 kcal / mol, according to quantum chemistry calculations. In the solid state, an 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. History In 1883, GABA was first synthesized, and it was first known only as a plant and microbe metabolic product. In 1950, GABA was discovered as an integral part of the mammalian central nervous system. Biosynthesis GABAergic neurons which produce GABA Exogenous GABA does not penetrate the blood -- brain barrier ; it is synthesized in the brain. It is synthesized from glutamate using the enzyme glutamate decarboxylase ( GAD ) and pyridoxal phosphate ( which is the active form of vitamin B6 ) as a cofactor. This process converts glutamate, the principal excitatory neurotransmitter, into the principal inhibitory neurotransmitter ( GABA ). GABA is converted back to glutamate by a metabolic pathway called the GABA shunt. Catabolism GABA transaminase enzyme catalyzes the conversion of 4 - aminobutanoic acid ( GABA ) and 2 - oxoglutarate ( α - ketoglutarate ) into succinic semialdehyde and glutamate. Succinic semialdehyde is then oxidized into succinic acid by succinic semialdehyde dehydrogenase and as such enters the citric acid cycle as a usable source of energy. Pharmacology Drugs that act as allosteric modulators of GABA receptors ( known as GABA analogues or GABAergic drugs ), or increase the available amount of GABA, typically have relaxing, anti-anxiety, and anti-convulsive effects. Many of the substances below are known to cause anterograde amnesia and retrograde amnesia. In general, GABA does not cross the blood -- brain barrier, although certain areas of the brain that have no effective blood -- brain barrier, such as the periventricular nucleus, can be reached by drugs such as systemically injected GABA. At least one study suggests that orally administered GABA increases the amount of human growth hormone ( HGH ). 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. Certain pro-drugs of GABA ( ex. picamilon ) have been developed to permeate the blood -- brain barrier, then separate into GABA and the carrier molecule once inside the brain. This allows for a direct increase of GABA levels throughout all areas of the brain, in a manner following the distribution pattern of the pro-drug prior to metabolism. GABA enhanced the catabolism of serotonin into N - acetylserotonin ( the precursor of melatonin ) in rats. It is thus suspected that GABA is involved in the synthesis of melatonin and thus might exert regulatory effects on sleep and reproductive functions. ( 1 ) Chemistry Although in chemical terms, GABA is an amino acid ( as it has both a primary amine and a carboxylic acid functional group ), it is rarely referred to as such in the professional, scientific, or medical community. By convention the term `` amino acid '', when used without a qualifier, refers specifically to an alpha amino acid. GABA is not an alpha amino acid, meaning the amino group is not attached to the alpha carbon so it is not incorporated into proteins. GABAergic drugs GABA receptor ligands. Agonists / positive allosteric modulators : alcohol ( ethanol ), barbiturates, benzodiazepines, carisoprodol, chloral hydrate, etaqualone, etomidate, glutethimide, kava, methaqualone, muscimol, neuroactive steroids, z - drugs, propofol, skullcap, valerian, theanine, volatile / inhaled anaesthetics. Antagonists / negative allosteric modulators : bicuculline, cicutoxin, flumazenil, furosemide, gabazine, oenanthotoxin, picrotoxin, Ro15 - 4513, thujone, amentoflavone. GABA receptor ligands. Agonists : baclofen, GBL, propofol, GHB, phenibut. Antagonists : phaclofen, saclofen. GABA reuptake inhibitors : deramciclane, hyperforin, tiagabine. GABA - transaminase inhibitors : gabaculine, phenelzine, valproate, vigabatrin, lemon balm ( Melissa officinalis ). 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PMID 17175815. Jump up ^ Dimitrijevic N, Dzitoyeva S, Satta R, Imbesi M, Yildiz S, Manev H ( 2005 ). `` Drosophila GABA receptors are involved in behavioral effects of gamma - hydroxybutyric acid ( GHB ) ''. Eur. J. Pharmacol. 519 ( 3 ) : 246 -- 252. doi : 10.1016 / j. ejphar. 2005.07. 016. PMID 16129424. Jump up ^ Awad R, Muhammad A, Durst T, Trudeau VL, Arnason JT ( August 2009 ). `` Bioassay - guided fractionation of lemon balm ( Melissa officinalis L. ) using an in vitro measure of GABA transaminase activity ''. Phytother Res. 23 ( 8 ) : 1075 -- 81. doi : 10.1002 / ptr. 2712. PMID 19165747. Jump up ^ Celikyurt IK, Mutlu O, Ulak G, Akar FY, Erden F ( 2011 ). `` Gabapentin, A GABA analogue, enhances cognitive performance in mice ''. Neuroscience Letters. 492 ( 2 ) : 124 -- 8. doi : 10.1016 / j. neulet. 2011.01. 072. PMID 21296127. Jump up ^ Park DH, Mirabella R, Bronstein PA, Preston GM, Haring MA, Lim CK, Collmer A, Schuurink RC ( October 2010 ). `` Mutations in γ - aminobutyric acid ( GABA ) transaminase genes in plants or Pseudomonas syringae reduce bacterial virulence ''. Plant J. 64 ( 2 ) : 318 -- 30. doi : 10.1111 / j. 1365 - 313X. 2010.04327. x. PMID 21070411. Jump up ^ Bouché N, Fromm H ( March 2004 ). `` GABA in plants : just a metabolite ? ''. Trends Plant Sci. 9 ( 3 ) : 110 -- 5. doi : 10.1016 / j. tplants. 2004.01. 006. PMID 15003233. Jump up ^ Roberts MR ( September 2007 ). `` Does GABA Act as a Signal in Plants ? : Hints from Molecular Studies ''. Plant Signal Behav. 2 ( 5 ) : 408 -- 9. doi : 10.4161 / psb. 2.5. 4335. PMC 2634229. PMID 19704616. Bibliography This section is empty. You can help by adding to it. ( October 2016 ) External links Media related to Gamma - Aminobutyric acid at Wikimedia Commons Parviz M, Vogel K, Gibson KM, Pearl PL ( 2014 - 11 - 25 ). `` GABA ''. Disorders of GABA metabolism : SSADH and GABA - transaminase deficiencies. Journal of Pediatric Epilepsy. 3 ( 4 ) : 217 -- 227. doi : 10.3233 / PEP - 14097. PMC 4256671. PMID 25485164. Clinical disorders known to affect inherited GABA metabolism Gamma - aminobutyric acid MS Spectrum Scholarpedia article on GABA List of GABA neurons on NeuroLex.org Neurotransmitters Amino acid - derived Major excitatory / inhibitory systems : Glutamate system : Agmatine Aspartic acid ( aspartate ) Cycloserine Glutamic acid ( glutamate ) Glutathione Glycine GSNO GSSG Kynurenic acid NAA NAAG Proline Serine ; GABA system : GABA GABOB GHB ; Glycine system : α - Alanine β - Alanine Glycine Hypotaurine Proline Sarcosine Serine Taurine ; GHB system : GHB T - HCA ( GHC ) Biogenic amines : Monoamines : 6 - OHM Dopamine Epinephrine ( adrenaline ) NAS ( normelatonin ) Norepinephrine ( noradrenaline ) Serotonin ( 5 - HT ) ; Trace amines : 3 - Iodothyronamine N - Methylphenethylamine N - Methyltryptamine m - Octopamine p - Octopamine Phenylethanolamine Phenethylamine Synephrine Tryptamine m - Tyramine p - Tyramine ; Others : Histamine Neuropeptides : See here instead. Lipid - derived Endocannabinoids : 2 - AG 2 - AGE ( noladin ether ) 2 - ALPI 2 - OG AA - 5 - HT Anandamide ( AEA ) DEA LPI NADA NAGly OEA Oleamide PEA RVD - Hpα SEA Virodhamine ( O - AEA ) Neurosteroids : See here instead. Nucleobase - derived Nucleosides : Adenosine system : Adenosine ADP AMP ATP Vitamin - derived Cholinergic system : Acetylcholine Miscellaneous Gasotransmitters : Carbon monoxide ( CO ) Hydrogen sulfide ( H S ) Nitric oxide ( NO ) ; Candidates : Acetaldehyde Ammonia ( NH ) Carbonyl sulfide ( COS ) Nitrous oxide ( N O ) Sulfur dioxide ( SO ) GABA receptor modulators Ionotropic GABA Agonists : ( + ) - Catechin Bamaluzole Barbiturates ( e.g., phenobarbital ) BL - 1020 DAVA Dihydromuscimol GABA Gabamide GABOB Gaboxadol ( THIP ) Homotaurine ( tramiprosate, 3 - APS ) Ibotenic acid iso - THAZ iso - THIP Isoguvacine Isomuscimol Isonipecotic acid Kojic amine Lignans ( e.g., honokiol ) Methylglyoxal Monastrol Muscimol Nefiracetam Neuroactive steroids ( e.g., allopregnanolone ) Org 20599 Phenibut Picamilon P4S Progabide Propofol Quisqualamine SL - 75102 TACA TAMP Terpenoids ( e.g., borneol ) Thiomuscimol Tolgabide ZAPA Positive modulators ( abridged ; see here for a full list ) : α - EMTBL Alcohols ( e.g., ethanol ) Anabolic steroids Avermectins ( e.g., ivermectin ) Barbiturates ( e.g., phenobarbital ) Benzodiazepines ( e.g., diazepam ) Bromide compounds ( e.g., potassium bromide ) Carbamates ( e.g., meprobamate ) Carbamazepine Chloralose Chlormezanone Clomethiazole Dihydroergolines ( e.g., ergoloid ( dihydroergotoxine ) ) Etazepine Etifoxine Fenamates ( e.g., mefenamic acid ) Flavonoids ( e.g., apigenin, hispidulin ) Fluoxetine Flupirtine Imidazoles ( e.g., etomidate ) Kava constituents ( e.g., kavain ) Lanthanum Loreclezole Monastrol Neuroactive steroids ( e.g., allopregnanolone, cholesterol ) Niacin Nicotinamide ( niacinamide ) Nonbenzodiazepines ( e.g., β - carbolines ( e.g., abecarnil ), cyclopyrrolones ( e.g., zopiclone ), imidazopyridines ( e.g., zolpidem ), pyrazolopyrimidines ( e.g., zaleplon ) ) Norfluoxetine Petrichloral Phenols ( e.g., propofol ) Phenytoin Piperidinediones ( e.g., glutethimide ) Propanidid Pyrazolopyridines ( e.g., etazolate ) Quinazolinones ( e.g., methaqualone ) Retigabine ( ezogabine ) ROD - 188 Skullcap constituents ( e.g., baicalin ) Stiripentol Sulfonylalkanes ( e.g., sulfonmethane ( sulfonal ) ) Topiramate Valerian constituents ( e.g., valerenic acid ) Volatiles / gases ( e.g., chloral hydrate, chloroform, diethyl ether, paraldehyde, sevoflurane ) Antagonists : Bicuculline Coriamyrtin Dihydrosecurinine Gabazine ( SR - 95531 ) Hydrastine Hyenachin ( mellitoxin ) PHP - 501 Pitrazepin Securinine Sinomenine SR - 42641 SR - 95103 Thiocolchicoside Tutin Negative modulators : 1, 3M1B 3M2B 11 - Ketoprogesterone 17 - Phenylandrostenol α5IA ( LS - 193,268 ) β - CCB β - CCE β - CCM β - CCP β - EMGBL Anabolic steroids Amiloride Anisatin β - Lactams ( e.g., penicillins, cephalosporins, carbapenems ) Basmisanil Bemegride Bilobalide CHEB Cicutoxin Cloflubicyne Cyclothiazide DHEA DHEA - S Dieldrin ( + ) - DMBB DMCM DMPC EBOB Etbicyphat FG - 7142 ( ZK - 31906 ) Fiproles ( e.g., fipronil ) Flavonoids ( e.g., amentoflavone, oroxylin A ) Flumazenil Fluoroquinolones ( e.g., ciprofloxacin ) Flurothyl Furosemide Iomazenil ( I ) Isoallopregnanolone Isopregnanolone ( sepranolone ) L - 655,708 Laudanosine Leptazol Lindane MaxiPost Morphine Morphine - 3 - glucuronide MRK - 016 Naloxone Naltrexone Nicardipine Nonsteroidal antiandrogens ( e.g., apalutamide, bicalutamide, enzalutamide, flutamide, nilutamide ) Oenanthotoxin Pentylenetetrazol ( pentetrazol ) Phenylsilatrane Picrotoxin ( i.e., picrotin and picrotoxinin ) Pregnenolone sulfate Propybicyphat PWZ - 029 Radequinil Ro 15 - 4513 Ro 19 - 4603 RO4882224 RO4938581 Sarmazenil SCS Suritozole TB - 21007 TBOB TBPS TCS - 1105 Terbequinil TETS Thujone U-93631 Zinc ZK - 93426 GABA - ρ Agonists : BL - 1020 CACA CAMP Homohypotaurine GABA GABOB Ibotenic acid Isoguvacine Muscimol N - Chloroacetylcytosine arabinoside Picamilon Progabide TACA TAMP Thiomuscimol Tolgabide Positive modulators : Allopregnanolone Alphaxolone ATHDOC Lanthanides Antagonists : ( S ) - 2 - MeGABA ( S ) - 4 - ACPBPA ( S ) - 4 - ACPCA 2 - MeTACA 3 - APMPA 4 - ACPAM 4 - GBA cis - 3 - ACPBPA CGP - 36742 ( SGS - 742 ) DAVA Gabazine ( SR - 95531 ) Gaboxadol ( THIP ) I4AA Isonipecotic acid Loreclezole P4MPA P4S SKF - 97541 SR - 95318 SR - 95813 TPMPA trans - 3 - ACPBPA ZAPA Negative modulators : 5α - Dihydroprogesterone Bilobalide Loreclezole Picrotoxin ( picrotin, picrotoxinin ) Pregnanolone ROD - 188 THDOC Zinc Metabotropic GABA Agonists : 1, 4 - Butanediol 4 - Fluorophenibut Aceburic acid Arbaclofen Arbaclofen placarbil Baclofen BL - 1020 GABA Gabamide GABOB GBL GHB GHBAL GHV GVL Isovaline Lesogaberan Phenibut Picamilon Progabide Sodium oxybate SKF - 97,541 SL 75102 Tolgabide Tolibut Positive modulators : ADX - 71441 BHF - 177 BHFF BSPP CGP - 7930 CGP - 13501 GS - 39783 rac - BHFF KK - 92A Antagonists : 2 - Hydroxysaclofen CGP - 35348 CGP - 46381 CGP - 52432 CGP - 54626 CGP - 55845 CGP - 64213 DAVA Homotaurine ( tramiprosate, 3 - APS ) Phaclofen Saclofen SCH - 50911 SKF - 97541 Negative modulators : Compound 14 See also Receptor / signaling modulators GABA receptor positive modulators GABA metabolism / transport modulators GABA metabolism and transport modulators Transporter GAT Inhibitors : 4 - Aminovaleric acid β - Alanine Arecaidine CI - 966 DABA Deramciclane ( EGIS - 3886, EGYT - 3886 ) EF - 1502 Gabaculine Guvacine Ibotenic acid Muscimol Nipecotic acid NNC 05 - 2090 NO - 711 Riluzole SKF - 89976A SNAP - 5114 TACA Tiagabine VIAAT Inhibitors : β - Alanine Bafilomycin A1 Chicago sky blue 6B Evans blue GABA Glycine N - Butyric acid Nigericin Nipecotic acid Valinomycin Vigabatrin Enzyme GAD Inhibitors : 3 - Mercaptopropionic acid AAOA L - Allylglycine Semicarbazide GABA - T Inhibitors : 3 - Hydrazinopropionic acid γ - Acetylenic - GABA AOAA EOS Gabaculine Isoniazid L - Cycloserine Phenelzine PEH Rosmarinic acid ( lemon balm ) Sodium valproate Valnoctamide Valproate pivoxil Valproate semisodium ( divalproex sodium ) Valproic acid Valpromide Vigabatrin Activators : 3 - Methyl - GABA See also Receptor / signaling modulators GABA receptor modulators GABA receptor positive modulators Glutamate metabolism / transport modulators GND : 4155919 - 8 NDL : 01112907 Retrieved from `` https://en.wikipedia.org/w/index.php?title=Gamma-Aminobutyric_acid&oldid=819005102 '' Categories : Neurotransmitters Amino acids GABA analogues GABA receptor agonists Glycine receptor agonists Biology of obsessive -- compulsive disorder Peripherally selective drugs GABA Non-proteinogenic amino acids Hidden categories : Wikipedia articles needing page number citations from May 2013 Articles needing additional medical references from June 2015 All articles needing additional references Articles needing expert attention with no reason or talk parameter Articles needing unspecified expert attention Articles needing expert attention from September 2016 All articles needing expert attention Articles with multiple maintenance issues Articles with changed EBI identifier ECHA InfoCard ID from Wikidata Articles containing unverified chemical infoboxes Chembox image size set All articles with specifically marked weasel - 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Question: a type of drug that works by enhancing the action of the neurotransmitter gaba
Answer: picamilon