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DC Field | Value | Language |
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dc.contributor.author | Delis, F. | en |
dc.contributor.author | Benveniste, H. | en |
dc.contributor.author | Xenos, M. | en |
dc.contributor.author | Grandy, D. | en |
dc.contributor.author | Wang, G. J. | en |
dc.contributor.author | Volkow, N. D. | en |
dc.contributor.author | Thanos, P. K. | en |
dc.date.accessioned | 2015-11-24T17:25:04Z | - |
dc.date.available | 2015-11-24T17:25:04Z | - |
dc.identifier.issn | 0145-6008 | - |
dc.identifier.uri | https://olympias.lib.uoi.gr/jspui/handle/123456789/12988 | - |
dc.rights | Default Licence | - |
dc.subject | d2 receptors | en |
dc.subject | ethanol | en |
dc.subject | brain | en |
dc.subject | mri | en |
dc.subject | mouse | en |
dc.subject | prenatal alcohol exposure | en |
dc.subject | matter volume loss | en |
dc.subject | gray-matter | en |
dc.subject | hippocampal volume | en |
dc.subject | agonists protect | en |
dc.subject | heavy drinking | en |
dc.subject | deficient mice | en |
dc.subject | brain volumes | en |
dc.subject | dependence | en |
dc.subject | individuals | en |
dc.title | Loss of Dopamine D2 Receptors Induces Atrophy in the Temporal and Parietal Cortices and the Caudal Thalamus of Ethanol-Consuming Mice | en |
heal.type | journalArticle | - |
heal.type.en | Journal article | en |
heal.type.el | Άρθρο Περιοδικού | el |
heal.identifier.primary | DOI 10.1111/j.1530-0277.2011.01667.x | - |
heal.identifier.secondary | <Go to ISI>://000303388500009 | - |
heal.identifier.secondary | http://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.language | en | - |
heal.access | campus | - |
heal.recordProvider | Πανεπιστήμιο Ιωαννίνων. Σχολή Θετικών Επιστημών. Τμήμα Μαθηματικών | el |
heal.publicationDate | 2012 | - |
heal.abstract | Background: 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.publisher | Wiley-Blackwell | en |
heal.journalName | Alcoholism-Clinical and Experimental Research | en |
heal.journalType | peer reviewed | - |
heal.fullTextAvailability | TRUE | - |
Appears in Collections: | Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά). ΜΑΘ |
Files in This Item:
File | Description | Size | Format | |
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Delis-2012-Loss of Dopamine D2.pdf | 421.62 kB | Adobe PDF | View/Open Request a copy |
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