Home Neuronal Signaling GABA Receptor agonist 4-Aminobutyric acid (GABA) For research use only.

4-Aminobutyric acid (GABA)

Synonyms: 4-Aminobutanoic acid, GABA, Gamma-aminobutyric acid, Piperidic acid

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

4-Aminobutyric acid (GABA) Chemical Structure

CAS: 56-12-2

Selleck's 4-Aminobutyric acid (GABA) has been cited by 1 publication

Purity & Quality Control

Batch: Purity: 99%
99

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Signaling Pathway

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GABA Receptor Signaling Pathway

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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
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].
Cell Research 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.
In Vivo
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].
Animal Research Animal Models Mice(CD1 mice) with STZ-induced diabetes
Dosages 20 μmol per mouse
Administration i.p.
NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT06057233 Not yet recruiting
Epilepsy Temporal Lobe
University Hospital Grenoble|Université Grenoble-Alpes|Institut National de la Santé Et de la Recherche Médicale France
 March 2024 --
NCT05995769 Not yet recruiting
Alcohol Use Disorder|Alcoholism
University of Calgary|Johns Hopkins University|University of Maryland|Canadian Institutes of Health Research (CIHR)
 January 2024 Phase 2
NCT04794335 Withdrawn
Inflammatory Bowel Diseases
University of Pittsburgh|National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
 November 1 2023 --

Chemical Information & Solubility

Molecular Weight 103.12 Formula

C4H9NO2
CAS No. 56-12-2 SDF Download 4-Aminobutyric acid (GABA) SDF
Smiles C(CC(=O)O)CN
Storage (From the date of receipt)

In vitro
Batch:

Water : 20 mg/mL

DMSO : Insoluble ( Moisture-absorbing DMSO reduces solubility. Please use fresh DMSO.)

Ethanol : Insoluble


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In vivo
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