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    Changes in dynorphin immunoreactivity but unaltered density of enkephalin immunoreactive neurons in basal ganglia nuclei of genetically dystonic hamsters (2011)

    Art
    Zeitschriftenartikel / wissenschaftlicher Beitrag
    Autoren
    Kreil, Annette
    Hamann, Melanie
    Sander, Svenja E
    Richter, Angelika
    Quelle
    Synapse; 65(11) — S. 1196–1203
    ISSN: 0887-4476
    Sprache
    Englisch
    Verweise
    DOI: 10.1002/syn.20959
    Pubmed: 21638337
    Kontakt
    Institut für Pharmakologie und Toxikologie

    Koserstr. 20
    14195 Berlin
    Tel.+49 30 838 53221 Fax.+49 30 838 53112
    email:pharmakologie@vetmed.fu-berlin.de

    Abstract / Zusammenfassung

    Dystonia is regarded as a basal ganglia disorder. In the dt(sz) hamster, a genetic animal model of paroxysmal dystonia, previous studies demonstrated a reduced density of striatal GABAergic interneurons which inhibit striatal GABAergic projection neurons. Although the disinhibition of striatal GABAergic projection neurons was evidenced in the dt(sz) hamster, alterations in their density have not been elucidated so far. Therefore, in the present study, the density of striatal methionin-(met-) enkephalin (ENK) immunoreactive GABAergic neurons, which project to the globus pallidus (indirect pathway), was determined in dt(sz) and control hamsters to clarify a possible role of an altered ratio between striatal interneurons and projection neurons. Furthermore, the immunoreactivity of dynorphin A (DYN), which is expressed in entopeduncular fibers of striatal neurons of the direct pathway, was verified by gray level measurements to illuminate the functional relevance of an enhanced striato-entopeduncular neuronal activity previously found in dt(sz) hamsters. While the density of striatal ENK immunoreactive (ENK(+) ) neurons did not significantly differ between mutant and control hamsters, there was a significantly enhanced ratio between the DYN immunoreactive area and the whole area of the EPN in dt(sz) hamsters compared to controls. These results support the hypothesis that a disbalance between a reduced density of striatal interneurons and an unchanged density of striatal projection neurons causes imbalances in the basal ganglia network. The consequentially enhanced striato-entopeduncular inhibition leads to an already evidenced reduced activity and an altered firing pattern of entopeduncular neurons in the dt(sz) hamster.