4aminobutyric

4-aminobutyric acid, often abbreviated as GABA, is a non-proteinogenic amino acid that functions as the principal inhibitory neurotransmitter in the central nervous system of mammals. The compound has the chemical formula C4H9NO2 and is composed of a four-carbon chain with an amino group on the fourth carbon and a carboxyl group on the first carbon. Historically, GABA was isolated in 1880 by French chemist Paul L. Brooke but its role as a neurotransmitter was discovered several decades later, in the 1960s, by G. S. Sheldon and colleagues.

In neural tissue, GABA binds to two main families of receptors: GABAA and GABAB. Activation of GABAA receptors, which are ligand-gated chloride channels, induces hyperpolarization of postsynaptic membranes, effectively dampening neuronal excitability. GABAB receptors are G-protein-coupled and inhibit adenylate cyclase, modulate ion channels, and reduce neurotransmitter release. The balance between excitatory signals, such as glutamate, and inhibitory GABAergic transmission is critical for processes like motor control, cognition, and the regulation of mood. Dysregulation of GABA signaling has been implicated in conditions such as epilepsy, anxiety disorders, insomnia, and schizophrenia.

Synthesized endogenously primarily via decarboxylation of glutamate catalyzed by glutamic acid decarboxylase (GAD), GABA levels can be altered by pharmacological agents. For instance, valproic acid increases GABA concentration by inhibiting its degradation, which underlies its anticonvulsant properties. Other compounds that modulate GABAergic activity include benzodiazepines, barbiturates, and neurosteroids. Despite its widespread importance, GABA cannot readily cross the blood–brain barrier; therefore, peripheral administration of GABA does not significantly raise central concentrations.