γ-aminobutyric acid

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Structural formula
Structural formula of gamma-aminobutyric acid
Surname γ- aminobutyric acid
other names
  • 4-aminobutyric acid
  • 4-aminobutanoic acid
  • Piperidic acid
  • γ- aminobutanoic acid
  • GABA
Molecular formula C 4 H 9 NO 2
Brief description

colorless solid

External identifiers / databases
CAS number 56-12-2
EC number 200-258-6
ECHA InfoCard 100,000,235
PubChem 119
ChemSpider 116
DrugBank DB02530
Wikidata Q210021
Molar mass 103.12 g mol −1
Physical state


Melting point

203 ° C (decomposition)

pK s value



very good in water (1300 g l −1 at 25 ° C)

safety instructions
GHS labeling of hazardous substances
07 - Warning


H and P phrases H: 315-319-335
P: 261-305 + 351 + 338
Toxicological data

12,680 mg kg −1 ( LD 50mouseoral )

As far as possible and customary, SI units are used. Unless otherwise noted, the data given apply to standard conditions .

The γ -aminobutyric acid (English gamma -Aminobutyric acid , abbreviated GABA ) more rarely, 4-aminobutyric acid or piperidine acid called, is a amine of butyric acid . The position of the amino group on the γ - carbon atom with respect to the carboxy group distinguishes it from the proteinogenic α - amino acids .

Biologically, γ- aminobutyric acid or GABA is an important endogenous messenger substance in many organisms , which is formed as a biogenic amine by decarboxylation of glutamic acid , especially by nerve cells . In the brain of adult mammals GABA is the major neurotransmitter of inhibitory (inhibitory) synapses ; During the fetal maturation phase, however, the effect is often excitatory.

Binding to GABAergic macromolecules

GABA binds to specific biological macromolecules. Thus enabled it ionotropic and metabotropic GABA receptors ; it passes through membranes via plasmalemmal (GAT) and vesicular (VGAT) transporters and is a substrate for transaminase.

The binding complex was characterized in more detail in 2018 using electron microscopy . In a predominantly stretched conformation , GABA binds with its amino group to loops B and C of the receptor subunit beta (β), namely via a salt bridge with glutamic acid (β- E 155), an aromatic cation-Pi bond (β-Y205) and a Hydrogen bond (β-Y97). The carboxy group of the ligand forms two hydrogen bonds (β-T202 and α-T129) and forms a salt bridge with the receptor subunit alpha (α) via arginine (α-R66). The ligand is stabilized in its position by surrounding aromatics (β-Y205, β-F200, β-Y157, α-F64). GABA also binds weakly to homologous binding sites α + / β-. When bound, GABA stabilizes the open conformation of the receptor, thus increasing the influx of anions and thus leading to a corresponding change in the membrane potential .

Biosynthesis and metabolism

GABA is produced in eukaryotic cells by the decarboxylation of glutamic acid using glutamate decarboxylase (GAD). This means that an excitatory neurotransmitter can become an inhibitory one in one step.

Biosynthesis of γ-aminobutyric acid

Receptors for GABA are often found on nerve cells and usually lead to an inhibition ( inhibition ) of nerve conduction. The neurotransmitter GABA can be reabsorbed by the presynaptic neuron and stored in synaptic vesicles for reuse. Some of the GABA molecules released into the synaptic gap as transmitters are taken up by neighboring glial cells . There the amino group is transferred to pyridoxal phosphate and further to α-ketoglutarate with the help of GABA transaminase ; the resulting succinate semialdehyde is metabolized via the citric acid cycle . This metabolism, located in the mitochondrial matrix and known as the GABA byway, is not restricted to the brain, but also exists in most other organs. With the help of the transaminase inhibitor vigabatrin , this breakdown path in the brain can be inhibited. This results in an increased GABA level with a protective effect against epileptic seizures .

GABA receptors play an important role in the development of neuronal structures in the brain. Interestingly, GABA often has an excitatory effect on newly formed neuronal connections in the fetus and thus contributes to their establishment.

GABA absorbed at the periphery only crosses the blood-brain barrier in small amounts. The effectiveness of GABA as a drug has not been proven; taking it for whatever purpose is therefore not recommended.

Role of GABA in the pancreas

GABA acts as an inhibitory transmitter in the pancreas by inhibiting the glucagon secretion of the alpha cells in the islets of Langerhans . GABA, produced bacterially in the gut of overfed obese mice, improved insulin secretion and decreased the accumulation of adipose tissue in the intestinal wall.

GABA modulators

In addition to the synthetic active substance gabazine, the plant poisons picrotoxin from the myrtle and bicuculline from the heart flowers are used as GABA antagonists for basic research . Muscimol , one of the poisons of the toadstool, is relevant as a GABA agonist . The active ingredient baclofen serves as an agonist in medical applications .

See also


  • H. Lüllmann, K. Mohr, M. Wehling: Pharmacology and Toxicology. 15th edition, Thieme Verlag, 2003, ISBN 3-13-368515-5 .
  • Klaus Aktories, Ulrich Förstermann, Franz Hofmann, Wolfgang Forth: General and special pharmacology and toxicology . 9th edition. Urban & Fischer, 2004, ISBN 3-437-42521-8 .
  • Robert M. Julien: Drugs and Psychotropic Drugs. Spektrum Akademischer Verlag, 1997, ISBN 3-8274-0044-9 .

Web links

Commons : Gamma-Aminobutyric acid  - Collection of pictures, videos and audio files
Wiktionary: Gamma-aminobutyric acid  - explanations of meanings, word origins, synonyms, translations
Wikibooks: Glutamate and Glutamine Metabolism  - Learning and Teaching Materials

Individual evidence

  1. Entry on AMINOBUTYRIC ACID in the CosIng database of the EU Commission, accessed on April 18, 2020.
  2. a b c data sheet γ-aminobutyric acid from Sigma-Aldrich , accessed on April 26, 2011 ( PDF ).
  3. a b c d Entry on γ-aminobutyric acid in the ChemIDplus database of the United States National Library of Medicine (NLM), accessed on July 31, 2018 or earlier.
  4. Phulera S, Zhu H, Yu J, Claxton DP, Yoder N, Yoshioka C, Gouaux E: Cryo-EM structure of the benzodiazepine-sensitive α1β1γ2S tri-heteromeric GABAA receptor in complex with GABA . In: Elife . July 7, 2018. doi : 10.7554 / eLife.39383 . PMID 30044221 . PMC 6086659 (free full text).
  5. Arne Schousbou and Helle S. Waagepetersen: Gamma-Aminobutyric Acid (GABA) in Encyclopedia of Neuroscience: Reference Module in Neuroscience and Biobehavioral Psychology 2009, pp. 511-515, doi : 10.1016 / B978-0-12-809324-5.02341- 5 .
  6. Michel Jung and Charles Danzin, New developments in enzyme-activated inhibitors of pyridoxal phosphate-dependent enzymes of therapeutic interest. in Design of Enzyme Inhibitors as Drugs pp. 257-293, Oxford University Press 1989.
  7. Lippert, B., Metcalf, BW, Jung, MJ and Casara, P .: 4-aminohex-5-enoic acid, a selective catalytic inhibitor of 4-aminobutyrate aminotransferase in mammalian brain. European Journal of Biochemistry No. 74, p. 441 (1977).
  8. ^ WH Oldendorf: Brain uptake of radiolabeled amino acids, amines, and hexoses after arterial injection . In: Am.J. Physiology Vol. 221 (1971), No. 6, pp. 1629-1639. doi : 10.1152 / ajplegacy.1971.221.6.1629 .
  9. Ada McVean, GABA supplements, glorious, gimmicky or just garbage? in McGill, Office of Science and Society. Separating sense from nonsense October 11, 2018.
  10. Anna Wendt, Bryndis Birnir, Karsten Buschard, Jesper Gromada, Albert Salehi, Sabine Sewing, Patrik Rorsman and Matthias Braun: Glucose Inhibition of Glucagon Secretion From Rat α-Cells Is Mediated by GABA Released From Neighboring β-Cells in Diabetes No. 53 , P. 1038 (2004)
  11. Patrik Rorsman, Per-Olof Berggren, Krister Bokvist, Hans Ericson, Hanns Möhler, Claes-Göran Östenson and Paul A. Smith: Glucose-inhibition of glucagon secretion involves activation of GABA A-receptor chloride channels in Nature No. 341, p . 233 (1989)
  12. Catherine Stanton et al .: Gamma-aminobutyric acidproducing lactobacilli positively affect metabolism and depressivelike behavior in a mouse model of metabolic syndrome. In: Nature Research, Scientific Reports No. 9, 2019, p. 16323, doi : 10.1038 / s41598-019-51781-x .
  13. ^ W. Bautista, J. Aguilar, JE Loeza-Alcocer, R. Delgado-Lezama: Pre- and postsynaptic modulation of monosynaptic reflex by GABAA receptors on turtle spinal cord. In: The Journal of Physiology. Volume 588/14, July 2010, pp. 2621-2631, doi : 10.1113 / jphysiol.2010.188979 , PMID 20519320 , PMC 2916992 (free full text).
  14. ^ Makoto Taketani: Advances in Network Electrophysiology. Springer Science & Business Media, 2006, ISBN 978-0-387-25858-4 , p. 305 ( limited preview in Google book search).
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