title: Glutamatergic pathways as a target for the treatment of dyskinesias in Parkinson's disease.
abstract: PD (Parkinson's disease) is characterized by some typical motor features that are caused by striatal dopamine depletion and respond well to dopamine-replacement therapy with L-dopa. Unfortunately, the majority of PD patients treated with L-dopa develop abnormal involuntary movements (dyskinesias) within a few years. The mechanisms underlying the development of LIDs (L-dopa-induced dyskinesias) involve, on one hand, a presynaptic dysregulation of dopamine release and clearance and, on the other hand, an abnormal postsynaptic response to dopamine in the brain. There is a large amount of evidence that these dopamine-dependent mechanisms are modulated by glutamatergic pathways and glutamate receptors. The present article summarizes the pathophysiological role of glutamatergic pathways in LID and reviews pre-clinical and clinical results obtained using pharmacological modulators of different classes and subtypes of glutamate receptors to treat parkinsonian dyskinesias.
authors.affiliation: *Basal Ganglia Pathophysiology Unit, Department of Experimental Medical Science, Lund University, BMC F11, 221 84 Lund, Sweden.
authors.forename: M Angela
authors.initials: MA
authors.lastname: Cenci
mesh_terms: D000818:Animals; D020820:Dyskinesias / Q000378:metabolism*; D004421:Dystonia / Q000378:metabolism; D006801:Humans; D007980:Levodopa / Q000627:therapeutic use; D019636:Neurodegenerative Diseases / Q000378:metabolism; D010300:Parkinson Disease / Q000378:metabolism*
chemical_list: D007980:Levodopa