Anterior cingulate gamma-aminobutyric acid concentrations and electroconvulsive therapy.

Autor: Erchinger VJ; Department of Clinical Medicine, University of Bergen, Bergen, Norway., Miller J; Department of Psychiatry, University of New Mexico School of Medicine, Albuquerque, NM, USA., Jones T; Department of Psychiatry, University of New Mexico School of Medicine, Albuquerque, NM, USA., Kessler U; Department of Clinical Medicine, University of Bergen, Bergen, Norway.; Division of Psychiatry, Haukeland University Hospital, Bergen, Norway., Bustillo J; Department of Psychiatry, University of New Mexico School of Medicine, Albuquerque, NM, USA., Haavik J; Division of Psychiatry, Haukeland University Hospital, Bergen, Norway.; Department of Biomedicine, University of Bergen, Bergen, Norway., Petrillo J; Department of Psychiatry, University of New Mexico School of Medicine, Albuquerque, NM, USA., Ziomek G; Department of Psychiatry, University of Texas at Austin Dell Medical School, Austin, TX, USA., Hammar Å; Division of Psychiatry, Haukeland University Hospital, Bergen, Norway.; Department of Biological and Medical Psychology, University of Bergen, Bergen, Norway., Oedegaard KJ; Department of Clinical Medicine, University of Bergen, Bergen, Norway., Calhoun VD; Tri-institutional Center for Translational Research in Neuroimaging and Data Science (TReNDS), Georgia Tech, Emory, Atlanta, GA, USA., McClintock SM; Division of Psychology, Department of Psychiatry, University of Texas Southwestern Medical Center, Dallas, TX, USA.; Division of Brain Stimulation and Neurophysiology, Department of Psychiatry and Behavioral Sciences, Duke University School of Medicine, Durham, NC, USA., Ersland L; Department of Biomedicine, University of Bergen, Bergen, Norway.; Department of Clinical Engineering, Haukeland University Hospital, Bergen, Norway.; Mohn Medical Imaging and Visualization Centre, Department of Radiology, Haukeland University Hospital, Bergen, Norway., Oltedal L; Department of Clinical Medicine, University of Bergen, Bergen, Norway.; Mohn Medical Imaging and Visualization Centre, Department of Radiology, Haukeland University Hospital, Bergen, Norway., Abbott CC; Department of Psychiatry, University of New Mexico School of Medicine, Albuquerque, NM, USA.
Jazyk: angličtina
Zdroj: Brain and behavior [Brain Behav] 2020 Nov; Vol. 10 (11), pp. e01833. Date of Electronic Publication: 2020 Sep 17.
DOI: 10.1002/brb3.1833
Abstrakt: 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 (t 71  = -0.36, p = .72) or in longitudinal analysis (t 36  = 0.97, p = .34). Remitters and nonremitters did not show longitudinal (t 36  = 1.12, p = .27) or cross-sectional differences in GABA+. GABA+ levels were not related to changes in antidepressant response (t 35  = 1.12, p = .27) or treatment number (t 36  = 0.05, p = .96). An association between cognitive performance and GABA+ levels was found in DEP that completed cognitive effortful testing (t 18  = 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.
(© 2020 The Authors. Brain and Behavior published by Wiley Periodicals LLC.)
Databáze: MEDLINE
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