The Lancet Neurology reports that levodopa, the drug used to treat the symptoms of Parkinson's disease, causes loss of function and dyskinesia with long-term use: being unable to control the limbs, with involuntary movements. Clinical studies suggest that pulsatile stimulation of the receptors on the receiving nerve cell causes dyskinesia, but the exact mechanism has not been clear until now.
In recent years, studies in animal models of Parkinson's disease have given important information about the molecular mechanisms at and beyond the receptor that lead to dyskinesia. New studies promise to focus on other mechanisms before and after the nerve junction (synapse): dopamine receptors, ions, metabotropic glutamate, and nerve signalling systems other than dopamine, and their role in dyskinesia.
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