Evidence for GABAergic inhibitory deficits in major depressive disorder.
Converging evidence suggests that deficits in gamma-aminobutyric acid (GABA) functioning are implicated in the pathophysiology of major depressive disorder (MDD). This is highlighted by research investigating cortical inhibition (CI), a process whereby GABAergic interneurons selectively attenuate pyramidal neurons. Transcranial magnetic stimulation (TMS) paradigms evaluate this marker of neuronal inhibitory activity in the cortex. This review will examine the neuroanatomic and neurophysiological evidence from neuroimaging, molecular, treatment, and TMS studies linking dysfunctional GABAergic neurotransmission to MDD.
Croarkin
Paul E
PE
Department of Psychiatry, UT Southwestern Medical Center Dallas, 6300 Harry Hines Boulevard, Suite 1200, Dallas, TX 75390-8589, USA. paul.croarkin@utsouthwestern.edu
Levinson
Andrea J
AJ
Daskalakis
Zafiris J
ZJ
D000818:Animals; D002540:Cerebral Cortex / Q000378:metabolism / Q000473:pathology; D003865:Major Depressive Disorder / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology*; D003952:Diagnostic Imaging; D006801:Humans; D009433:Neural Inhibition / Q000502:physiology*; D009482:Neurophysiology; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
D005680:gamma-Aminobutyric Acid