4-Aminobutyric acid

Research use only, not for human use.

The most common inhibitory neurotransmitter in the central nervous system.

The most common inhibitory neurotransmitter in the central nervous system. (In Vitro):γ-Aminobutyric acid (30 μM) depolarizes cortical progenitor cells (E16 cells), results an inward current in ventricular zone (VZ) cells, and induces DNA synthesis inhibition, with half-maximal response concentration of 5 μM.Cortical plate (cp) neurons expresses glutamic acid decarboxylase (GAD), γ-Aminobutyric acid (1-5 μM; 18 h) stimulates the motility and arrests the migration of cp cells, while the chemotropic signal is involved G-protein activation.γ-Aminobutyric acid activates GABA A receptors, causing cell cycle arrest in S phase and limiting growth.(In Vivo):γ-Aminobutyric acid (33.95, 102.25, 306.75 mg/kg; p.o.; single dose) can enhance the sleep of mice.γ-Aminobutyric acid (1, 2, 4 mg/kg/d; p.o.; 30 d) alleviates anxiety and restored food utilization rate in rats, with impairment induced by Di(2-ethylhexyl) phthalate (DEHP) exposure.

γ-Aminobutyric acid (30 μM) depolarizes cortical progenitor cells (E16 cells), results an inward current in ventricular zone (VZ) cells, and induces DNA synthesis inhibition, with half-maximal response concentration of 5 μM.Cortical plate (cp) neurons expresses glutamic acid decarboxylase (GAD), γ-Aminobutyric acid (1-5 μM; 18 h) stimulates the motility and arrests the migration of cp cells, while the chemotropic signal is involved G-protein activation.γ-Aminobutyric acid activates GABA A receptors, causing cell cycle arrest in S phase and limiting growth. Cell Migration Assay Cell Line:Cortical plate (cp) neurons Concentration:1-5 μM Incubation Time:18 hoursResult:Promoted motility via G-protein activation and arrested attractantinduced migration via GABAA receptor-mediated depolarization.

γ-Aminobutyric acid (33.95, 102.25, 306.75 mg/kg; p.o.; single dose) can enhance the sleep of mice.γ-Aminobutyric acid (1, 2, 4mg/kg/d; p.o.; 30 d) alleviates anxiety and restored food utilization rate in rats, with impairment induced by Di(2-ethylhexyl) phthalate (DEHP) exposure. Animal Model:Pathogens free (SPF) Bagg’s albino (Balb/c) mice (18–20 g, 8 weeks old)Dosage:33.95, 102.25, 306.75 mg/kg Administration:Oral gavage; single dose; 20 mL/kg administration; measured in an hour Result:Prolonged the sleep duration, increased sleep rate, and shorten the sleep latency more effectively.Animal Model:Sprague-Dawley rat indued by DEHP (HY-B1945) (500 mg/kg)Dosage:1, 2, 4?mg/kg Administration:Oral gavage; combined administration; for 30 consecutive days Result:Reduced the levels of nitric oxide and nitric oxide synthase in rats treated with DEHP.

Aminalon | DF 468 | DF468 | DF-468 | Mielogen | Mielomade | Gamma-aminobutyric acid

Membrane Transporter/Ion Channel

GAT

GABA

Neurological Disease

——

56-12-2

103.12

C4H9NO2

>98% (HPLC)

Soluble in DMSO

O=C(O)CCCN

4-aminobutanoic acid

(-20℃)

With Ice Pack

≥ 2 years