γ-Aminobutyric acid

γ-Aminobutyric acid belongs to natural products and functions as an agonist of GABAA and GABAB receptors, possessing central sedative effects, cell permeability, and the ability to modulate neuronal excitability. This compound is used in neuroscience research and exhibits anxiolytic, anticonvulsant, and neuroprotective activities.

Methods: GABRP-positive pancreatic cancer cells (KLM-1, PK-45P) and HEK293 cells with exogenous GABRP expression were treated with γ-Aminobutyric acid (GABA) (1–100 μM), with intervention by GABAA receptor antagonists; proliferation was detected by MTT assay and BrdU incorporation, intracellular Ca²⁺ was measured by Fura-2, and Erk phosphorylation was detected by Western blot.
Results: γ-Aminobutyric acid (GABA) dose-dependently promoted cell proliferation, elevated intracellular Ca²⁺, and activated the Erk pathway; these effects were inhibited by GABAA receptor antagonists. [1]
Methods: INS-1 cells and mouse primary islet β-cells were treated with γ-Aminobutyric acid (GABA) (100 μM); membrane potential was recorded by patch-clamp, Ca²⁺ influx was detected by Fura-2 calcium imaging, and Akt phosphorylation was detected by Western blot.
Results: γ-Aminobutyric acid (GABA) induced membrane depolarization and Ca²⁺ influx in β-cells, activated the PI3K/Akt pathway, exerting pro-survival and anti-diabetic effects. [2]

Methods: MDSD and NOD diabetic mice received daily intraperitoneal injections of GABA (20 μmol per mouse) for several weeks; blood glucose was monitored with a glucometer, and circulating insulin and glucagon levels were detected by RIA.
Results: γ-Aminobutyric acid (GABA) treatment increased circulating insulin, decreased glucagon, maintained near-normal blood glucose levels, and significantly improved metabolic status in mice. [2]
Methods: SJL/J mice were immunized with PLP 139-151 to induce EAE models; GABAergic drugs topiramate (100 mg/kg) or vigabatrin (400 mg/kg) were administered orally daily, dissolved in PBS, for 37 consecutive days or starting from the disease peak. Cytokines were detected by ELISA, and spinal cord inflammation was assessed by H&E staining.
Results: GABAergic drugs significantly reduced EAE clinical scores, inhibited IL-1β and IL-6 production in macrophages and IFN-γ and IL-17 production in T cells, and decreased central inflammatory infiltration. [3]

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.(Only for Reference)

H2O: 100 mg/mL (969.74 mM), Sonication is recommended.

DMSO: Insoluble