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|Place of Origin:||China|
|Certification:||ISO, GMP, Kosher|
|Minimum Order Quantity:||50kgs|
|Packaging Details:||T/T L/C|
|Delivery Time:||5-8 work days|
|Supply Ability:||100 Tons Per Year|
|Other Name:||γ－Aminobutyric Acid||Appearance::||White Fine Powder|
|Molecular Mass:||103.1||Shelf Life:||Two Years|
Product Name: Amma-Aminobutyric acid
As a chemical substance, GABA was artificially synthesized as early as 1883. In 1950, the concentration of GABA in normal brain of mammals was found to be high, but its physiological significance was unknown. Subsequently, an extract was extracted from bovine brain which could inhibit crayfish stretch receptor neurons to produce impulse. It was found that the extract had anti-acetylcholine effect and contraction effect on the ileum of the guinea pigs and rabbits. It was proved that GABA was the inhibitory component in the extract. Segal SA and others also confirmed that GABA had a general inhibitory effect on mammalian central nervous system. Injecting GABA separated by ion electrophoresis into the neurons around the cat's cortical cruciate sulcus could induce hyperpolarization of neurons. Its potential was the same as that produced by stimulating the synapses on the cortical surface, and electrical stimulation was found. The GABA content in the fourth ventricular perfusion fluid of the cat's cerebellum tripled, and it was speculated that the chemical transmitter released by the Purkinje neurons was GABA.
Specification: 20% 99% HPLC
Molecular Formula: C4H9NO2
Molecular Mass: 103.1
CAS No.: 56-12-2
amma-Aminobutyric acid (γ-Aminobutyric acid) (GABA) is the chief inhibitory neurotransmitter in the mammalian central nervous system. Its principal role is reducing neuronal excitability throughout the nervous system. In humans, GABA is also directly responsible for the regulation of muscle tone. While GABA is an inhibitory transmitter in the mature brain, its actions were thought to be primarily excitatory in the developing brain. The gradient of chloride was reported to be reversed in immature neurons, with its reversal potential higher than the resting membrane potential of the cell; activation of a GABA-A receptor thus leads to efflux of Cl−ions from the cell (that is, a depolarizing current). The differential gradient of chloride in immature neurons was shown to be primarily due to the higher concentration of NKCC1 co-transporters relative to KCC2 co-transporters in immature cells. GABA itself is partially responsible for orchestrating the maturation of ion pumps. GABAergic interneurons mature faster in the hippocampus and the GABA signalling machinery appears earlier than glutamatergic transmission. Thus, GABA was considered the major excitatory neurotransmitter in many regions of the brain before the maturation of glutamatergic synapses.