Loss of Dopamine D2 Receptors Induces Atrophy in the Temporal and Parietal Cortices and the Caudal Thalamus of Ethanol-Consuming Mice

dc.contributor.authorDelis, F.en
dc.contributor.authorBenveniste, H.en
dc.contributor.authorXenos, M.en
dc.contributor.authorGrandy, D.en
dc.contributor.authorWang, G. J.en
dc.contributor.authorVolkow, N. D.en
dc.contributor.authorThanos, P. K.en
dc.date.accessioned2015-11-24T17:25:04Z
dc.date.available2015-11-24T17:25:04Z
dc.identifier.issn0145-6008-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/12988
dc.rightsDefault Licence-
dc.subjectd2 receptorsen
dc.subjectethanolen
dc.subjectbrainen
dc.subjectmrien
dc.subjectmouseen
dc.subjectprenatal alcohol exposureen
dc.subjectmatter volume lossen
dc.subjectgray-matteren
dc.subjecthippocampal volumeen
dc.subjectagonists protecten
dc.subjectheavy drinkingen
dc.subjectdeficient miceen
dc.subjectbrain volumesen
dc.subjectdependenceen
dc.subjectindividualsen
dc.titleLoss of Dopamine D2 Receptors Induces Atrophy in the Temporal and Parietal Cortices and the Caudal Thalamus of Ethanol-Consuming Miceen
heal.abstractBackground: The need of an animal model of alcoholism becomes apparent when we consider the genetic diversity of the human populations, an example being dopamine D2 receptor (DRD2) expression levels. Research suggests that low DRD2 availability is associated with alcohol abuse, while higher DRD2 levels may be protective against alcoholism. This study aims to establish whether (i) the ethanol-consuming mouse is a suitable model of alcohol-induced brain atrophy and (ii) DRD2 protect the brain against alcohol toxicity. Methods: Adult Drd2+/+ and Drd2-/- mice drank either water or 20% ethanol solution for 6 months. At the end of the treatment period, the mice underwent magnetic resonance (MR) imaging under anesthesia. MR images were registered to a common space, and regions of interest were manually segmented. Results: We found that chronic ethanol intake induced a decrease in the volume of the temporal and parietal cortices as well as the caudal thalamus in Drd2-/- mice. Conclusions: The result suggests that (i) normal DRD2 expression has a protective role against alcohol-induced brain atrophy and (ii) in the absence of Drd2 expression, prolonged ethanol intake reproduces a distinct feature of human brain pathology in alcoholism, the atrophy of the temporal and parietal cortices.en
heal.accesscampus-
heal.fullTextAvailabilityTRUE-
heal.identifier.primaryDOI 10.1111/j.1530-0277.2011.01667.x-
heal.identifier.secondary<Go to ISI>://000303388500009-
heal.identifier.secondaryhttp://onlinelibrary.wiley.com/store/10.1111/j.1530-0277.2011.01667.x/asset/j.1530-0277.2011.01667.x.pdf?v=1&t=h3b5rf3s&s=d6b39523539af260feeb66fb9617967b15b7b517-
heal.journalNameAlcoholism-Clinical and Experimental Researchen
heal.journalTypepeer reviewed-
heal.languageen-
heal.publicationDate2012-
heal.publisherWiley-Blackwellen
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Θετικών Επιστημών. Τμήμα Μαθηματικώνel
heal.typejournalArticle-
heal.type.elΆρθρο Περιοδικούel
heal.type.enJournal articleen

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