• 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. |