The dopaminergic system in dyskinesia
| • Striatal dopamine depletion is not a prerequisite for development of dyskinesia, if high doses of l-DOPA are administered. |
| • Pulsatile dopamine replacement therapy appears as a key etiological factor in the development of LID. |
| • Initial therapy with longer-lasting dopaminergic agents can delay the onset of dyskinesia. |
| • Continuous delivery of dopamine agonists or l-DOPA can reduce the severity of established dyskinesia. |
| • Dopamine receptor supersensitivity. |
| • Overactive D1-mediated neurotransmission. |
| • Recruitment of D1 receptors at the synaptic membrane. |
| • Lentiviral-induced internalization of D1 receptors alleviates LI-AIMs in the 6-OHDA-lesioned rat and LID in the MPTP-lesioned NHP. |
| • Each of D1, D2, and D3 receptors are involved in the development and expression of dyskinesia. |
| • Cross-talk between D1 and D3 receptors. |