Abstract:   γ-aminobutyric acid (GABA) is the most important inhibitory amino acid neurotransmitter in the central nervous system to maintain the excitatory-inhibitory balance of the brain. Increasing clinical and pre-clinical evidence shows a central and causal role of GABAergic deficits in depressive disorders. Depressive patients commonly indicate reduced GABAergic transmission in emotional and cognitive brain areas, especially prefrontal cortex and limbic areas like hippocampus and amygdala, and antidepressants can alleviate or reverse depressive symptoms by augmenting GABAergic activity in these areas. Furthermore, deficits in GABAergic transmission are sufficient to cause most of the neural and behavioral alterations expected in an animal model of depression. GABAergic system undergoes a prolonged development to structural and functional maturation until into early adulthood in both human and rodents. Stress, especially early stress, may disturb the mature trajectory of the GABAergic system, and result in continuing negative consequences of neural development and late functioning, which can contribute to the increased susceptibility for the onset of depression across late life. It would be important to further elucidate GABAergic mechanisms underlying depressive disorders and action of antidepressant in order to improve strategy for early recognition and intervention of depression.

Key words: stress, GABAergic, depression