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pubmed-article:11425506pubmed:abstractTextPrevious work has suggested that the therapeutic efficacy of olanzapine might be partially dependent on action at the D(1)-dopamine (DA) receptor site. Because early DA loss can lead to supersensitive D(1)-DA receptors, effects of olanzapine were investigated in adult rats given lesions to DA-containing neurons as neonates. In these animals, locomotor effects of SKF-38393 (a D(1)-DA agonist) were attenuated by olanzapine, but at doses (5 and 10 mg/kg) that decreased activity when given alone. Olanzapine prevented induction of striatal Fos protein by SKF-38393 and partially attenuated the long-term "priming" effect of repeated SKF-38393 treatment. Olanzapine also antagonized the stimulant effects of quinpirole (a D(2)-type DA agonist) in animals lesioned as young adults, at doses lower than those necessary to antagonize SKF-38393-induced activity. In addition, olanzapine antagonized apomorphine-induced self-injurious behavior in neonate-lesioned rats in a dose-related fashion. Attenuation of self-injury in this animal model suggests that olanzapine should be tested against this symptom in patient populations.lld:pubmed
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pubmed-article:11425506pubmed:dateRevised2011-5-18lld:pubmed
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pubmed-article:11425506pubmed:articleTitleEffect of olanzapine on functional responses from sensitized D1-dopamine receptors in rats with neonatal dopamine loss.lld:pubmed
pubmed-article:11425506pubmed:affiliationDepartment of Psychiatry, Skipper Bowles Center for Alcohol Studies, University of North Carolina School of Medicine, Chapel Hill 27599-7178, USA. sheryl.moy@css.unc.edulld:pubmed
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