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dc.contributor.authorSteiner, Johann
dc.contributor.authorWalter, Martin
dc.contributor.authorGos, Tomasz
dc.contributor.authorGuillemin, Gilles J
dc.contributor.authorBernstein, Hans-Gert
dc.contributor.authorSarnyai, Zoltán
dc.contributor.authorMawrin, Christian
dc.contributor.authorBrisch, Ralf
dc.contributor.authorBielau, Hendrik
dc.contributor.authorMeyer zu Schwabedissen, Louise
dc.contributor.authorBogerts, Bernhard
dc.contributor.authorMyint, Aye-Mu
dc.date.accessioned2011-09-23T17:09:24Z
dc.date.available2011-09-23T17:09:24Z
dc.date.issued2011-08-10
dc.identifierhttp://dx.doi.org/10.1186/1742-2094-8-94
dc.identifier.issn1742-2094
dc.identifier.urihttp://www.dspace.cam.ac.uk/handle/1810/239025
dc.descriptionRIGHTS : This article is licensed under the BioMed Central licence at http://www.biomedcentral.com/about/license which is similar to the 'Creative Commons Attribution Licence'. In brief you may : copy, distribute, and display the work; make derivative works; or make commercial use of the work - under the following conditions: the original author must be given credit; for any reuse or distribution, it must be made clear to others what the license terms of this work are.
dc.description.abstractBACKGROUND: Immune dysfunction, including monocytosis and increased blood levels of interleukin-1, interleukin-6 and tumour necrosis factor α has been observed during acute episodes of major depression. These peripheral immune processes may be accompanied by microglial activation in subregions of the anterior cingulate cortex where depression-associated alterations of glutamatergic neurotransmission have been described. METHODS: Microglial immunoreactivity of the N-methyl-D-aspartate (NMDA) glutamate receptor agonist quinolinic acid (QUIN) in the subgenual anterior cingulate cortex (sACC), anterior midcingulate cortex (aMCC) and pregenual anterior cingulate cortex (pACC) of 12 acutely depressed suicidal patients (major depressive disorder/MDD, n = 7; bipolar disorder/BD, n = 5) was analyzed using immunohistochemistry and compared with its expression in 10 healthy control subjects. RESULTS: Depressed patients had a significantly increased density of QUIN-positive cells in the sACC (P = 0.003) and the aMCC (P = 0.015) compared to controls. In contrast, counts of QUIN-positive cells in the pACC did not differ between the groups (P = 0.558). Post-hoc tests showed that significant findings were attributed to MDD and were absent in BD. CONCLUSIONS: These results add a novel link to the immune hypothesis of depression by providing evidence for an upregulation of microglial QUIN in brain regions known to be responsive to infusion of NMDA antagonists such as ketamine. Further work in this area could lead to a greater understanding of the pathophysiology of depressive disorders and pave the way for novel NMDA receptor therapies or immune-modulating strategies.
dc.publisherSpringer Science and Business Media LLC
dc.rightsAll Rights Reserved
dc.rights.urihttps://www.rioxx.net/licenses/all-rights-reserved/
dc.titleSevere depression is associated with increased microglial quinolinic acid in subregions of the anterior cingulate gyrus: evidence for an immune-modulated glutamatergic neurotransmission?
dc.typeArticle
dc.date.updated2011-09-23T17:09:24Z
dc.description.versionPeer Reviewed
dc.language.rfc3066en
dc.rights.holderSteiner et al.; licensee BioMed Central Ltd.
prism.publicationNameJ Neuroinflammation
pubs.declined2017-10-11T13:54:31.162+0100
dcterms.dateAccepted2011-08-10
rioxxterms.versionofrecord10.1186/1742-2094-8-94
dc.identifier.eissn1742-2094


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