Modulation of the basal ganglia dopaminergic system in a transgenic mouse exhibiting dystonia-like features
Autor: | Ioanna A. Armata, Panagiotis Giompres, Dimitra Giannakopoulou, Ada Mitsacos, Pullani Shashidharan |
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Rok vydání: | 2010 |
Předmět: |
Male
medicine.medical_specialty Dopamine Mice Transgenic Substantia nigra Striatum Biology Basal Ganglia Article Mice Internal medicine Neural Pathways Basal ganglia medicine Animals Humans Genetic Predisposition to Disease Biological Psychiatry Dystonia Pars compacta Dopaminergic medicine.disease Disease Models Animal Psychiatry and Mental health Endocrinology Neurology Neurology (clinical) medicine.symptom Hyperkinesia medicine.drug |
Zdroj: | Journal of Neural Transmission. 117:1401-1409 |
ISSN: | 1435-1463 0300-9564 |
Popis: | Dystonia is a movement disorder characterized by involuntary excessive muscle activity and abnormal postures. There are data supporting the hypothesis that basal ganglia dysfunction, and specifically dopaminergic system dysfunction, plays a role in dystonia. In the present study, we used hyperkinetic transgenic mice generated as a model of DYT1 dystonia and compared the basal ganglia dopaminergic system between transgenic mice exhibiting hyperkinesia (affected), transgenic mice not showing movement abnormalities (unaffected), and non-transgenic littermates. A decrease in the density of striatal D2 binding sites, measured by [³H]raclopride binding, and D2 mRNA expression in substantia nigra pars compacta (SNpc) was revealed in affected and unaffected transgenic mice when compared with non-transgenic. No difference in D1 receptor binding and DAT binding, measured by [³H]SCH23390 and [³H]WIN35428 binding, respectively, was found in striatum of transgenic animals. In SNpc, increased levels of DAT binding sites were observed in affected and unaffected animals compared to non-transgenic, whereas no change in DAT mRNA expression was found. Our results show selective neurochemical changes in the basal ganglia dopaminergic system, suggesting a possible involvement in the pathophysiology of dystonia-like motor hyperactivity. |
Databáze: | OpenAIRE |
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