Anterior cingulate gamma‐aminobutyric acid concentrations and electroconvulsive therapy
Abstract 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 macro...
| Main Authors: | , , , , , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Wiley
2020-11-01
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| Series: | Brain and Behavior |
| Subjects: | |
| Online Access: | https://doi.org/10.1002/brb3.1833 |
| _version_ | 1818436921500631040 |
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| author | Vera J. Erchinger Jeremy Miller Thomas Jones Ute Kessler Juan Bustillo Jan Haavik Jonathan Petrillo Gregory Ziomek Åsa Hammar Ketil J. Oedegaard Vince D. Calhoun Shawn M. McClintock Lars Ersland Leif Oltedal Christopher C. Abbott |
| author_facet | Vera J. Erchinger Jeremy Miller Thomas Jones Ute Kessler Juan Bustillo Jan Haavik Jonathan Petrillo Gregory Ziomek Åsa Hammar Ketil J. Oedegaard Vince D. Calhoun Shawn M. McClintock Lars Ersland Leif Oltedal Christopher C. Abbott |
| author_sort | Vera J. Erchinger |
| collection | DOAJ |
| description | Abstract 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. |
| first_indexed | 2024-12-14T17:16:28Z |
| format | Article |
| id | doaj.art-652dfdfadac14266b855b7cff3d54fc2 |
| institution | Directory Open Access Journal |
| issn | 2162-3279 |
| language | English |
| last_indexed | 2024-12-14T17:16:28Z |
| publishDate | 2020-11-01 |
| publisher | Wiley |
| record_format | Article |
| series | Brain and Behavior |
| spelling | doaj.art-652dfdfadac14266b855b7cff3d54fc22022-12-21T22:53:24ZengWileyBrain and Behavior2162-32792020-11-011011n/an/a10.1002/brb3.1833Anterior cingulate gamma‐aminobutyric acid concentrations and electroconvulsive therapyVera J. Erchinger0Jeremy Miller1Thomas Jones2Ute Kessler3Juan Bustillo4Jan Haavik5Jonathan Petrillo6Gregory Ziomek7Åsa Hammar8Ketil J. Oedegaard9Vince D. Calhoun10Shawn M. McClintock11Lars Ersland12Leif Oltedal13Christopher C. Abbott14Department of Clinical Medicine University of Bergen Bergen NorwayDepartment of Psychiatry University of New Mexico School of Medicine Albuquerque NM USADepartment of Psychiatry University of New Mexico School of Medicine Albuquerque NM USADepartment of Clinical Medicine University of Bergen Bergen NorwayDepartment of Psychiatry University of New Mexico School of Medicine Albuquerque NM USADivision of Psychiatry Haukeland University Hospital Bergen NorwayDepartment of Psychiatry University of New Mexico School of Medicine Albuquerque NM USADepartment of Psychiatry University of Texas at Austin Dell Medical School Austin TX USADivision of Psychiatry Haukeland University Hospital Bergen NorwayDepartment of Clinical Medicine University of Bergen Bergen NorwayTri‐institutional Center for Translational Research in Neuroimaging and Data Science (TReNDS) Georgia Tech Emory Atlanta GA USADivision of Psychology Department of Psychiatry University of Texas Southwestern Medical Center Dallas TX USADepartment of Biomedicine University of Bergen Bergen NorwayDepartment of Clinical Medicine University of Bergen Bergen NorwayDepartment of Psychiatry University of New Mexico School of Medicine Albuquerque NM USAAbstract 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.https://doi.org/10.1002/brb3.1833depressionelectroconvulsive therapygamma‐aminobutyric acidmagnetic resonance spectroscopy |
| spellingShingle | Vera J. Erchinger Jeremy Miller Thomas Jones Ute Kessler Juan Bustillo Jan Haavik Jonathan Petrillo Gregory Ziomek Åsa Hammar Ketil J. Oedegaard Vince D. Calhoun Shawn M. McClintock Lars Ersland Leif Oltedal Christopher C. Abbott Anterior cingulate gamma‐aminobutyric acid concentrations and electroconvulsive therapy Brain and Behavior depression electroconvulsive therapy gamma‐aminobutyric acid magnetic resonance spectroscopy |
| title | Anterior cingulate gamma‐aminobutyric acid concentrations and electroconvulsive therapy |
| title_full | Anterior cingulate gamma‐aminobutyric acid concentrations and electroconvulsive therapy |
| title_fullStr | Anterior cingulate gamma‐aminobutyric acid concentrations and electroconvulsive therapy |
| title_full_unstemmed | Anterior cingulate gamma‐aminobutyric acid concentrations and electroconvulsive therapy |
| title_short | Anterior cingulate gamma‐aminobutyric acid concentrations and electroconvulsive therapy |
| title_sort | anterior cingulate gamma aminobutyric acid concentrations and electroconvulsive therapy |
| topic | depression electroconvulsive therapy gamma‐aminobutyric acid magnetic resonance spectroscopy |
| url | https://doi.org/10.1002/brb3.1833 |
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