Journal article
Glutamate and Gamma-Aminobutyric Acid Systems in the Pathophysiology of Major Depression and Antidepressant Response to Ketamine
Biological psychiatry (1969), Vol.81(10), pp.886-897
05/15/2017
DOI: 10.1016/j.biopsych.2016.05.005
PMCID: PMC5107161
PMID: 27449797
Abstract
In patients with major depressive disorder or bipolar disorder, abnormalities in excitatory and/or inhibitory neurotransmission and neuronal plasticity may lead to aberrant functional connectivity patterns within large brain networks. Network dysfunction in association with altered brain levels of glutamate and gamma-aminobutyric acid have been identified in both animal and human studies of depression. In addition, evidence of an antidepressant response to subanesthetic-dose ketamine has led to a collection of studies that have examined neurochemical (e.g., glutamatergic and gamma-aminobutyric acidergic) and functional imaging correlates associated with such an effect. Results from these studies suggest that an antidepressant response in association with ketamine occurs, in part, by reversing these neurochemical/physiological disturbances. Future studies in depression will require a combination of neuroimaging approaches from which more biologically homogeneous subgroups can be identified, particularly with respect to treatment response biomarkers of glutamatergic modulation.
Details
- Title: Subtitle
- Glutamate and Gamma-Aminobutyric Acid Systems in the Pathophysiology of Major Depression and Antidepressant Response to Ketamine
- Creators
- Marc S Lener - Experimental Therapeutics and Pathophysiology Branch, Intramural Research Program, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland. Electronic address: marc.lener@nih.govMark J Niciu - Experimental Therapeutics and Pathophysiology Branch, Intramural Research Program, National Institute of Mental Health, National Institutes of Health, Bethesda, MarylandElizabeth D Ballard - Experimental Therapeutics and Pathophysiology Branch, Intramural Research Program, National Institute of Mental Health, National Institutes of Health, Bethesda, MarylandMinkyung Park - Experimental Therapeutics and Pathophysiology Branch, Intramural Research Program, National Institute of Mental Health, National Institutes of Health, Bethesda, MarylandLawrence T Park - Experimental Therapeutics and Pathophysiology Branch, Intramural Research Program, National Institute of Mental Health, National Institutes of Health, Bethesda, MarylandAllison C Nugent - Experimental Therapeutics and Pathophysiology Branch, Intramural Research Program, National Institute of Mental Health, National Institutes of Health, Bethesda, MarylandCarlos A Zarate Jr - Experimental Therapeutics and Pathophysiology Branch, Intramural Research Program, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland
- Resource Type
- Journal article
- Publication Details
- Biological psychiatry (1969), Vol.81(10), pp.886-897
- DOI
- 10.1016/j.biopsych.2016.05.005
- PMID
- 27449797
- PMCID
- PMC5107161
- NLM abbreviation
- Biol Psychiatry
- ISSN
- 0006-3223
- eISSN
- 1873-2402
- Publisher
- United States
- Grant note
- Z99 MH999999 / Intramural NIH HHS ZIA MH002857 / Intramural NIH HHS
- Language
- English
- Date published
- 05/15/2017
- Academic Unit
- Psychiatry; Iowa Neuroscience Institute
- Record Identifier
- 9984003470102771
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