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English: Possible pathophysiology of levodopa-induced dyskinesia. The pathophysiology of levodopa-induced dyskinesia could be classified into three levels. The first is cortical level, the second is presynapses within striatum, and the third is postsynapses within striatum. At the cortical level, it has an abnormal cortical plasticity resulting the abnormal of glutamatergic output to the striatum. Subsequently, at the presynaptic level, there are many alterations such as loss of striatal presynaptic dopaminergic terminal and increasing the role of presynaptic serotoninergic terminal. When these alterations are occurred coupling with administration of levodopa, the pulsatile release of the dopamine might occur. Another presynaptic alteration is the alteration of activity of endocannabinoid receptors that might increase the glutamatergic activity. According to the postsynaptic alterations, there is increased activity of dopaminergic receptor, especially on D1 receptor and increasing the activity of both metabotropic and ionotropic glutamatergic receptors. The result of the alterations of all levels is changing the intracellular signaling pathway leading to increase the phosphorylation that creates the abnormal synaptic plasticity in term of losing the ability to create the depotentiation. Finally, the onset of inappropriate control of motor function and the dyskinesia occurs