Acute restraint stress induces specific changes in nitric oxide production and inflammatory markers in the rat hippocampus and striatum

Chen, Hsiao-Jou Cortina, Spiers, Jereme G., Sernia, Conrad and Lavidis, Nickolas A. (2016) Acute restraint stress induces specific changes in nitric oxide production and inflammatory markers in the rat hippocampus and striatum. Free Radical Biology and Medicine, 90 219-229. doi:10.1016/j.freeradbiomed.2015.11.023


Author Chen, Hsiao-Jou Cortina
Spiers, Jereme G.
Sernia, Conrad
Lavidis, Nickolas A.
Title Acute restraint stress induces specific changes in nitric oxide production and inflammatory markers in the rat hippocampus and striatum
Journal name Free Radical Biology and Medicine   Check publisher's open access policy
ISSN 1873-4596
0891-5849
Publication date 2016-01-01
Year available 2015
Sub-type Article (original research)
DOI 10.1016/j.freeradbiomed.2015.11.023
Open Access Status Not Open Access
Volume 90
Start page 219
End page 229
Total pages 11
Place of publication Philadelphia, PA, United States
Publisher Elsevier
Language eng
Formatted abstract
Chronic mild stress has been shown to cause hippocampal neuronal nitric oxide synthase (NOS) overexpression and the resultant nitric oxide (NO) production has been implicated in the etiology of depression. However, the extent of nitrosative changes including NOS enzymatic activity and the overall output of NO production in regions of the brain like the hippocampus and striatum following acute stress has not been characterized. In this study, outbred male Wistar rats aged 6-7 weeks were randomly allocated into 0 (control), 60, 120, or 240 min stress groups and neural regions were cryodissected for measurement of constitutive and inducible NOS enzymatic activity, nitrosative status, and relative gene expression of neuronal and inducible NOS. Hippocampal constitutive NOS activity increased initially but was superseded by the inducible isoform as stress duration was prolonged. Interestingly, hippocampal neuronal NOS and interleukin-1β mRNA expression was downregulated, while the inducible NOS isoform was upregulated in conjunction with other inflammatory markers. This pro-inflammatory phenotype within the hippocampus was further confirmed with an increase in the glucocorticoid-antagonizing macrophage migration inhibitory factor, Mif, and the glial surveillance marker, Ciita. This indicates that despite high levels of glucocorticoids, acute stress sensitizes a neuroinflammatory response within the hippocampus involving both pro-inflammatory cytokines and inducible NOS while concurrently modulating the immunophenotype of glia. Furthermore, there was a delayed increase in striatal inducible NOS expression while no change was found in other pro-inflammatory mediators. This suggests that short term stress induces a generalized increase in inducible NOS signaling that coincides with regionally specific increased markers of adaptive immunity and inflammation within the brain.
Keyword Acute stress
Hippocampus
Nitric oxide
Nitric oxide synthase
Pro-inflammatory cytokines
Redox status
Striatum
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Official 2016 Collection
School of Biomedical Sciences Publications
 
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Created: Sun, 06 Dec 2015, 22:43:06 EST by Cortina Chen on behalf of School of Biomedical Sciences