The thorny problem of dyskinesias: Dendritic Spines, synaptic plasticity, and striatal dysfunction

摘要

Abnormal involuntary movements, particularly levodopa-induced dyskinesia (LID) and antipsychotic drug-elicited tardive dyskinesia, are among the most difficult to manage adverse effects associated with the treatment of Parkinson's disease (PD) and schizophrenia, respectively. The mechanisms underlying dyskinesias in levodopa-treated PD have been studied for decades. Over this time, there has been a gradual shift from a focus on mechanisms associated with surviving dopamine (presynaptic) neurons to changes in dopaminoceptive cells in the striatum.