4-Aminobutyric acid (GABA)

Catalog No.S4700 Synonyms: 4-Aminobutanoic acid, GABA, Gamma-aminobutyric acid, Piperidic acid

For research use only.

4-Aminobutyric acid (4-Aminobutanoic acid, GABA, Gamma-aminobutyric acid, Piperidic acid) is a naturally occurring neurotransmitter with central nervous system (CNS) inhibitory activity.

4-Aminobutyric acid (GABA) Chemical Structure

CAS No. 56-12-2

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Biological Activity

Description 4-Aminobutyric acid (4-Aminobutanoic acid, GABA, Gamma-aminobutyric acid, Piperidic acid) is a naturally occurring neurotransmitter with central nervous system (CNS) inhibitory activity.
Targets
GABA receptor [1]
In vitro

γ-Aminobutyric acid (GABA) functions primarily as an inhibitory neurotransmitter in the mature central nervous system. The addition of GABA into the cell culture medium promoted the proliferation of GABRP-expressing PDAC cells, but not GABRP-negative cells, and GABAA receptor antagonists inhibited this growth-promoting effect by GABA. The HEK293 cells constitutively expressing exogenous GABRP revealed the growth-promoting effect of GABA treatment. GABA treatment in GABRP-positive cells increased intracellular Ca2+ levels and activated the mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/Erk) cascade[1]. GABA exerts antidiabetic effects by acting on both the islet β-cells and immune system. Unlike in adult brain or islet α-cells in which GABA exerts hyperpolarizing effects, in islet β-cells, GABA produces membrane depolarization and Ca2+ influx, leading to the activation of PI3K/Akt-dependent growth and survival pathways[2].

In vivo GABA is the principal inhibitory neurotransmitter in the adult brain that has a parallel inhibitory role in the immune system. GABAergic medications are used to treat anxiety, alcohol withdrawal, epilepsy, and to induce sedation, and anesthesia. GABA is neuroprotective in animal models of stroke. GABA treatment decreases inflammatory cytokine production in peripheral macrophages. It decreases T cell autoimmunity and the development of inflammatory responses in the nonobese diabetic mouse model of type 1 diabetes[3]. In the adult brain, GABA induces a fast inhibition in neurons mainly through the GABAA receptor (GABAAR). GABA is produced by pancreatic β-cells. GABA released from β-cells can act on GABAAR in the α-cells, causing membrane hyperpolarization and hence suppressing glucagon secretion. GABA-treated mice showed higher circulating insulin, lower glucagon, nearly normal glycemia, improved metabolic conditions, and maintained close to normal glucose tolerance during a period of 53 d after STZ injections[2].

Protocol (from reference)

Cell Research:[1]
  • Cell lines: PDAC cell lines KLM-1, SUIT-2, KP-1N, PK-1, PK-45P, and PK-59
  • Concentrations: 0, 1, 10, 100 μmol/L
  • Incubation Time: 6 days
  • Method: GABRP-positive cell lines, KLM-1 and PK-45P, and GABRP-negative cell lines, PK-59 and KP-1N, are incubated with GABA or GABA receptor agonist Muscimol at serial concentration (0, 1, 10, 100 μmol/L) in appropriate medium supplemented with 1% FBS for 6 days. To inhibit the GABA-mediated pathway, cells are incubated with 250 μmol/L of GABAA receptor antagonist bicuculline methiodide or 1 mmol/L of GABAB receptor antagonist CGP-35348. After 6 days of exposure to either of these drugs, cell viability is measured by MTT assay as described above.
Animal Research:[2]
  • Animal Models: Mice(CD1 mice) with STZ-induced diabetes
  • Dosages: 20 μmol per mouse
  • Administration: i.p.

Solubility (25°C)

In vitro

Chemical Information

Molecular Weight 103.12
Formula

C4H9NO2

CAS No. 56-12-2
Storage 3 years -20°C powder
2 years -80°C in solvent
Smiles C(CC(=O)O)CN

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Clinical Trial Information

NCT Number Recruitment Interventions Conditions Sponsor/Collaborators Start Date Phases
NCT04299828 Not yet recruiting Other: Discarded blood samples Congenital Heart Disease|Coagulation Boston Children''s Hospital December 2022 --
NCT04823364 Not yet recruiting Other: Neurotransmitters evaluation by MRS Attention Deficit Disorder With Hyperactivity Weizmann Institute of Science|Tel Aviv University|Maccabi Healthcare Services Israel October 1 2022 Not Applicable
NCT04532190 Not yet recruiting Device: rTMS Attention-Deficit/Hyperactivity Disorder (ADHD) University of Calgary August 31 2022 Not Applicable
NCT05459090 Not yet recruiting Other: ex-vivo study Drug Resistant Epilepsy Neuromed IRCCS August 1 2022 --
NCT04794335 Not yet recruiting -- Inflammatory Bowel Diseases University of Pittsburgh|National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) July 1 2022 --
NCT05317546 Not yet recruiting Drug: Cannabidiol Alcohol Use Disorder Medical University of South Carolina July 2022 Phase 2

(data from https://clinicaltrials.gov, updated on 2022-08-01)

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