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Research Investigator Profile
Interactions between dopaminergic and glutamatergic systems in the striatum are thought to underlie the pathology, symptoms as well as adverse effects of long-term treatment of Parkinson’s disease patients with dopaminergic drugs.
Previous studies from our group have revealed that in a rodent model of Parkinson’s disease, the expression, assembly and phosphorylation of NMDA receptors are altered in the striatum. Further work resulted in the discovery of a dopamine receptor-dependent mechanism for the trafficking of striatal NMDA receptors between intracellular and post-synaptic compartments.
The current research focus involves exploring the mechanisms and signaling pathways by which dysregulation of NMDA receptor functions causes parkinsonism and dyskinesias using in vivo and in vitro models. Modification of these molecular pathways may constitute a useful therapeutic target for Parkinson’s disease and dyskinesia, including other basal ganglia disorders where abnormal functions of NMDA receptors in the striatum contribute significantly to the symptoms of the diseases.
Synaptic basis of neurodegenerative diseases such as Parkinson's and Huntington's
Molecular, Genetic, Immunocytochemistry, Confocal Microscopy, Fluorescence Lifetime Imaging Microscopy, Biochemical and Pharmacological Techniques, Stereotaxic 6-OHDA Model of PD, Culturing Neurons
Parkinson's and Huntington's diseases
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