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

Foteini Delis, Helene Benveniste, Michalis Xenos, David Grandy, Gene Jack Wang, Nora D. Volkow, Panayotis K. Thanos

    Research output: Contribution to journalArticle

    4 Scopus citations

    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 6months. 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.

    Original languageEnglish (US)
    Pages (from-to)815-825
    Number of pages11
    JournalAlcoholism: Clinical and Experimental Research
    Volume36
    Issue number5
    DOIs
    StatePublished - May 2012

    Keywords

    • Brain
    • D2 Receptors
    • Ethanol
    • MRI
    • Mouse

    ASJC Scopus subject areas

    • Medicine (miscellaneous)
    • Toxicology
    • Psychiatry and Mental health

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