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    Impaired spatial memory and altered dendritic spine morphology in angiotensin II type 2 receptor-deficient mice (2008)

    Art
    Zeitschriftenartikel / wissenschaftlicher Beitrag
    Autoren
    Maul, Björn
    von Bohlen und Halbach, Oliver
    Becker, Axel
    Sterner-Kock, Anja
    Voigt, Jörg-Peter
    Siems, Wolf-Eberhard
    Grecksch, Gisela
    Walther, Thomas
    Quelle
    Journal of molecular medicine : JMM ; official organ of the Gesellschaft Deutscher Naturforscher und Ärzte; 86(5) — S. 563–71
    ISSN: 0946-2716
    Sprache
    Englisch
    Verweise
    DOI: 10.1007/s00109-008-0316-4
    Pubmed: 18335189
    Kontakt
    Institut für Pharmakologie und Toxikologie

    Koserstr. 20
    14195 Berlin
    +49 30 838 53221
    pharmakologie@vetmed.fu-berlin.de

    Abstract / Zusammenfassung

    Mental retardation is the most frequent cause of serious handicap in children and young adults. Mutations in the human angiotensin II type 2 receptor (AT2) have been implicated in X-linked forms of mental retardation. We here demonstrate that mice lacking the AT2 receptor gene are significantly impaired in their performance in a spatial memory task and in a one-way active avoidance task. As no difference was observed between the genotypes in fear conditioning, the detected deficit in spatial memory may not relate to fear. Notably, receptor knockout mice showed increased motility in an activity meter and elevated plus maze. Importantly, these mice are characterized by abnormal dendritic spine morphology and length, both features also found to be associated with some cases of mental retardation. These findings suggest a crucial role of AT2 in normal brain function and that dysfunction of the receptor has impact on brain development and ultrastructural morphology with distinct consequences on learning and memory.