Abstract
Chronic L-dopa administration is associated with development of dyskinesias. The molecular mechanisms of these side-effects, however, remain elusive. Dopamine (DA) receptors interact with other receptors to form highly organized complexes where their activity is finely tuned by several proteins. The DA D1R forms a heteromeric complex with the NMDA receptor (NMDAR) and this interaction influences the trafficking of both receptors. Using the 6-hydroxydopamine rat model of Parkinson's disease, we report a correlation between the development of L-dopa-induced dyskinesias and changes in synaptic D1R/NMDAR complexes.
Publication types
-
Research Support, Non-U.S. Gov't
-
Review
MeSH terms
-
Adrenergic Agents / toxicity
-
Animals
-
Antiparkinson Agents / adverse effects*
-
Disease Models, Animal
-
Dyskinesia, Drug-Induced / etiology*
-
Dyskinesia, Drug-Induced / metabolism*
-
Humans
-
Levodopa / adverse effects*
-
Models, Molecular
-
Oxidopamine / toxicity
-
Parkinson Disease / drug therapy
-
Parkinson Disease / etiology
-
Protein Subunits / analysis
-
Protein Subunits / metabolism
-
Rats
-
Receptors, Dopamine / metabolism*
-
Receptors, N-Methyl-D-Aspartate / metabolism*
Substances
-
Adrenergic Agents
-
Antiparkinson Agents
-
Protein Subunits
-
Receptors, Dopamine
-
Receptors, N-Methyl-D-Aspartate
-
Levodopa
-
Oxidopamine