Journal
WORLD JOURNAL OF BIOLOGICAL PSYCHIATRY
Volume 20, Issue 5, Pages 381-392Publisher
TAYLOR & FRANCIS LTD
DOI: 10.1080/15622975.2017.1371332
Keywords
Depression; glutamate; slc7a11; system xc-; N-acetylcysteine
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Funding
- Fund for Scientific Research Flanders (FWO) [G. 038412N]
- Queen Elisabeth Medical Foundation
- Vrije Universiteit Brussel [SRP40]
- agency for Innovation by Science and Technology (IWT)
- FWO
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Objectives: The cystine/glutamate antiporter (system xc-) is believed to contribute to nonvesicular glutamate release from glial cells in various brain areas. Although recent investigations implicate system xc- in mood disorders, unambiguous evidence has not yet been established. Therefore, we evaluated the possible role of system xc- in the depressive state. Methods: We conducted a protein expression analysis of the specific subunit of system xc- (xCT) in brain regions of the corticosterone mouse model, Flinders Sensitive Line rat model and post-mortem tissue of depressed patients. We next subjected system xc- deficient mice to the corticosterone model and analysed their behaviour in several tests. Lastly, we subjected additional cohorts of xCT-deficient and wild-type mice to N-acetylcysteine treatment to unveil whether the previously reported antidepressant-like effects are dependent upon system xc-. Results: We did not detect any changes in xCT expression levels in the animal models or patients compared to proper controls. Furthermore, loss of system xc- had no effect on depression- and anxiety-like behaviour. Finally, the antidepressant-like effects of N-acetylcysteine are not mediated via system xc-. Conclusions: xCT protein expression is not altered in the depressed brain and system xc- deficiency does not affect depression-associated behaviour in the corticosterone mouse model.
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