Objective: The anticonvulsant hypothesis posits that ECT’s mechanism of action is related to enhancement of endogenous anticonvulsant brain mechanisms. Results of prior studies investigating the role of the inhibitory neurotransmitter gamma-aminobutyric acid (“GABA+”, GABA and coedited macromolecules) in the pathophysiology and treatment of depression remain inconclusive. The aim of our study was to investigate treatment-responsive changes of GABA+ in subjects with a depressive episode receiving electroconvulsive therapy (ECT). Methods: In total, 41 depressed subjects (DEP) and 35 healthy controls (HC) were recruited at two independent sites in Norway and the USA. MEGA-PRESS was used for investigation of GABA+ in the anterior cingulate cortex. We assessed longitudinal and cross-sectional differences between DEP and HC, as well as the relationship between GABA+ change and change in depression severity and number of ECTs. We also assessed longitudinal differences in cognitive performance and GABA+ levels. Results: Depressive episode did not show a difference in GABA+ relative to HC (t71 = −0.36, p =.72) or in longitudinal analysis (t36 = 0.97, p =.34). Remitters and nonremitters did not show longitudinal (t36 = 1.12, p =.27) or cross-sectional differences in GABA+. GABA+ levels were not related to changes in antidepressant response (t35 = 1.12, p =.27) or treatment number (t36 = 0.05, p =.96). An association between cognitive performance and GABA+ levels was found in DEP that completed cognitive effortful testing (t18 = 2.4, p =.03). Conclusion: Our results failed to support GABA as a marker for depression and abnormal mood state and provide no support for the anticonvulsant hypothesis of ECT. ECT-induced change in GABA concentrations may be related to change in cognitive function.
- electroconvulsive therapy
- gamma-aminobutyric acid
- magnetic resonance spectroscopy
ASJC Scopus subject areas
- Behavioral Neuroscience