Gamma-aminobutyric acid (GABA) (GABA)

Gamma-aminobutyric acid (GABA) is the primary inhibitory neurotransmitter in the mammalian central nervous system and a critical mediator of the gut-brain axis (Strandwitz et al., 2019). While GABA is synthesized endogenously in the brain, significant quantities are produced by commensal gut microbiota, particularly species within the genera Bacteroides, Bifidobacterium, and Lactobacillus (Yunes et al., 2016). This microbially derived GABA can influence host physiology by interacting with GABA receptors on the enteric nervous system or by signaling through the vagus nerve to modulate brain function, mood, and stress responses (Bravo et al., 2011). Dysregulation of the GABAergic system and the gut-brain axis is implicated in various psychiatric and neurological conditions, including anxiety, depression, and irritable bowel syndrome (Cryan & Dinan, 2012). Therapeutic strategies, such as the use of psychobiotics, aim to modulate GABA levels by introducing specific GABA-producing bacterial strains or prebiotics to restore neurological balance. Pharmacologically, the GABAergic system is targeted by a wide range of drugs, including benzodiazepines and GABA-B agonists, which enhance receptor activity to produce sedative, anxiolytic, and muscle-relaxant effects.

Other names

4-aminobutanoic acidgamma-aminobutyrateMicrobial GABAGut-derived GABA

GABA acts as the primary inhibitory neurotransmitter by binding to and activating GABA-A (ionotropic chloride channels) and GABA-B (metabotropic G protein-coupled) receptors. Activation of GABA-A receptors leads to an influx of chloride ions, while GABA-B activation increases potassium efflux, both resulting in neuronal hyperpolarization and reduced firing. In the gut-brain axis, microbially produced GABA can stimulate the vagus nerve or act on the enteric nervous system to transmit inhibitory signals to the central nervous system.