Evidence for GABAergic inhibitory deficits in major depressive disorder

Neurosci Biobehav Rev. 2011 Jan;35(3):818-25. doi: 10.1016/j.neubiorev.2010.10.002. Epub 2010 Oct 12.


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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Cerebral Cortex / metabolism
  • Cerebral Cortex / pathology
  • Depressive Disorder, Major / metabolism*
  • Depressive Disorder, Major / pathology
  • Depressive Disorder, Major / physiopathology*
  • Diagnostic Imaging
  • Humans
  • Neural Inhibition / physiology*
  • Neurophysiology
  • gamma-Aminobutyric Acid / metabolism*


  • gamma-Aminobutyric Acid