4-aminobutyrate aminotransferase (GABA transaminase) (ABAT)

The GABA transaminase and the associated catabolism and uptake system constitute the primary mechanisms for terminating the action of gamma-aminobutyric acid (GABA), the major inhibitory neurotransmitter in the central nervous system [1][2]. 4-aminobutyrate aminotransferase (GABA-T) is a mitochondrial enzyme that catalyzes the degradation of GABA into succinate semialdehyde, while GABA transporters (GATs) mediate the reuptake of GABA from the synaptic cleft into neurons and astrocytes [1][5]. Together, these components are vital for maintaining GABAergic tone and preventing neuronal hyperexcitability [6]. Pharmacological modulation of this system is a cornerstone of epilepsy treatment; for instance, vigabatrin irreversibly inhibits GABA-T, and tiagabine blocks GAT-1, both resulting in increased synaptic GABA concentrations [3][7]. While effective for seizure control and infantile spasms, targeting this system can lead to significant side effects, including sedation and, specifically for vigabatrin, permanent peripheral visual field defects [3].

Other names

GABA-TGABAT4-aminobutyrate:2-oxoglutarate aminotransferaseGABA catabolic systemGABA uptake systemGAT-1SLC6A1

Elevation of synaptic GABA levels through the irreversible inhibition of its metabolic degradation by GABA transaminase or the blockade of its reuptake by GABA transporters [3][7].