4-Aminobutyric acid (GABA)

Catalog No.S4700 Batch:S470001

Technical Data

Formula	C₄H₉NO₂
Molecular Weight	103.12	CAS No.	56-12-2
Solubility (25°C)*	In vitro	Water	20 mg/mL (193.94 mM)
		DMSO	Insoluble
		Ethanol	Insoluble
* <1 mg/ml means slightly soluble or insoluble. * Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations. * Room temperature shipping (Stability testing shows this product can be shipped without any cooling measures.)

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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 Assay:^{^[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 Study:^{^[2]}	Animal Models Mice(CD1 mice) with STZ-induced diabetes Dosages 20 μmol per mouse Administration i.p.

Cell Assay:^{^[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 Study:^{^[2]}

Animal Models
Mice(CD1 mice) with STZ-induced diabetes
Dosages
20 μmol per mouse
Administration
i.p.

References

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

The delta subunit of the GABAA receptor is necessary for the GPT2-promoted breast cancer metastasis [ Theranostics, 2023, 13(4):1355-1369]	PubMed: 36923530

The delta subunit of the GABAA receptor is necessary for the GPT2-promoted breast cancer metastasis [ Theranostics, 2023, 13(4):1355-1369]

PubMed: 36923530

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SHIPPING AND STORAGE
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