The omega-3 polyunsaturated fatty acid docosahexaenoic acid (DHA) reverses corticosterone-induced changes in cortical neurons

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dc.contributor.author Pusceddu, Matteo M.
dc.contributor.author Nolan, Yvonne M.
dc.contributor.author Green, Holly F.
dc.contributor.author Robertson, Ruairi C.
dc.contributor.author Stanton, Catherine
dc.contributor.author Kelly, Philip M.
dc.contributor.author Cryan, John F.
dc.contributor.author Dinan, Timothy G.
dc.date.accessioned 2017-03-08T15:14:09Z
dc.date.available 2017-03-08T15:14:09Z
dc.date.issued 2015-12-12
dc.identifier.citation Pusceddu, M. M., Nolan, Y. M., Green, H. F., Robertson, R. C., Stanton, C., Kelly, P., Cryan, J. F. and Dinan, T. G. (2016) 'The Omega-3 Polyunsaturated Fatty Acid Docosahexaenoic Acid (DHA) Reverses Corticosterone-Induced Changes in Cortical Neurons', International Journal of Neuropsychopharmacology, 19(6), pyv130. doi:10.1093/ijnp/pyv130 en
dc.identifier.volume 9 en
dc.identifier.issued 6 en
dc.identifier.startpage pyv130-1 en
dc.identifier.endpage pyv130-10 en
dc.identifier.issn 1469-5111
dc.identifier.uri http://hdl.handle.net/10468/3759
dc.identifier.doi 10.1093/ijnp/pyv130
dc.description.abstract Background: Chronic exposure to the glucocorticoid hormone corticosterone exerts cellular stress-induced toxic effects that have been associated with neurodegenerative and psychiatric disorders. Docosahexaenoic acid is a polyunsaturated fatty acid that has been shown to be of benefit in stress-related disorders, putatively through protective action in neurons. Methods: We investigated the protective effect of docosahexaenoic acid against glucocorticoid hormone corticosterone-induced cellular changes in cortical cell cultures containing both astrocytes and neurons. Results: We found that glucocorticoid hormone corticosterone (100, 150, 200 μM) at different time points (48 and 72 hours) induced a dose- and time-dependent reduction in cellular viability as assessed by methyl thiazolyl tetrazolium. Moreover, glucocorticoid hormone corticosterone (200 μM, 72 hours) decreased the percentage composition of neurons while increasing the percentage of astrocytes as assessed by βIII-tubulin and glial fibrillary acidic protein immunostaining, respectively. In contrast, docosahexaenoic acid treatment (6 μM) increased docosahexaenoic acid content and attenuated glucocorticoid hormone corticosterone (200 μM)-induced cell death (72 hours) in cortical cultures. This translates into a capacity for docosahexaenoic acid to prevent neuronal death as well as astrocyte overgrowth following chronic exposure to glucocorticoid hormone corticosterone. Furthermore, docosahexaenoic acid (6 μM) reversed glucocorticoid hormone corticosterone-induced neuronal apoptosis as assessed by terminal deoxynucleotidyl transferase–mediated nick-end labeling and attenuated glucocorticoid hormone corticosterone-induced reductions in brain derived neurotrophic factor mRNA expression in these cultures. Finally, docosahexaenoic acid inhibited glucocorticoid hormone corticosterone-induced downregulation of glucocorticoid receptor expression on βIII- tubulin-positive neurons. Conclusions: This work supports the view that docosahexaenoic acid may be beneficial in ameliorating stress-related cellular changes in the brain and may be of value in psychiatric disorders. en
dc.description.sponsorship Department of Agriculture, Food and the Marine (Food Institutional Research Measure, FIRM (grant number 10/RD/TMFRC/709)); Science Foundation Ireland (centre grant (Alimentary Pharmabiotic Centre grant no. SFI/12/RC/2273), Investigator Award (grant no. 12/IA/1537)) en
dc.format.mimetype application/pdf en
dc.language.iso en en
dc.publisher Oxford University Press en
dc.rights © The Authors 2015. Published by Oxford University Press on behalf of CINP. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com en
dc.rights.uri http://creativecommons.org/licenses/by-nc/4.0/ en
dc.subject Docosahexaenoic acid en
dc.subject Corticosterone en
dc.subject Stress en
dc.subject Glucocorticoid receptors en
dc.subject Brain derived neurotrophic factor en
dc.title The omega-3 polyunsaturated fatty acid docosahexaenoic acid (DHA) reverses corticosterone-induced changes in cortical neurons en
dc.type Article (peer-reviewed) en
dc.internal.authorcontactother John F Cryan, Department Of Anatomy & Neuroscience, University College Cork, Cork, Ireland. +353-21-490-3000 Email: j.cryan@ucc.ie en
dc.internal.availability Full text available en
dc.date.updated 2017-03-08T14:36:34Z
dc.description.version Published Version en
dc.internal.rssid 349552320
dc.internal.pmid 26657646
dc.contributor.funder Science Foundation Ireland en
dc.contributor.funder Department of Agriculture, Food and the Marine en
dc.description.status Peer reviewed en
dc.identifier.journaltitle International Journal of Neuropsychopharmacology en
dc.internal.copyrightchecked No !!CORA!! en
dc.internal.licenseacceptance Yes en
dc.internal.IRISemailaddress j.cryan@ucc.ie en


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© The Authors 2015. Published by Oxford University Press on behalf of CINP. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com Except where otherwise noted, this item's license is described as © The Authors 2015. Published by Oxford University Press on behalf of CINP. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com
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