Priming and expression of L-dopa-induced dyskinesia (LID) is associated with maladaptive plasticity of striatal spiny projection neurons (SPNs) in the direct pathway of the basal ganglia. The L-dopa dosage threshold for dyskinesia decreases immediately after dopaminergic denervation, then gradually after repeated L-dopa treatment. Dopaminergic denervation induces D1 receptor hypersensitivity in the soma and axon terminals and diminishes negative feedback from GABAB receptors in the direct pathway SPNs, resulting in neuronal hypersensitivity. After dopaminergic denervation, serotonergic neurons metabolize L-dopa. Serotonergic neurons do not have D2 receptors or dopamine transporters, resulting in a non-regulated release of dopamine, with subsequent pulsatile dopamine receptor stimulation. L-dopa treatment post-dopaminergic denervation induces LID in rat models. Dyskinetic rats show a lack of depotentiation at their corticostriatal synapses and enlargement of their dendritic spines within direct pathway SPNs, both of which account for strengthened corticostriatal synaptic transmission in LID models. Intra-SPN signal transduction is activated, resulting in the hypersynthesis of GABA. The volume of the internal segment of the globus pallidus (GPi) increases alongside the enlargement of axon terminals with many synaptic vesicles containing GABA from direct pathway SPNs. When the model expresses LID, excessive GABA is released into the GPi. LID priming involves excessive GABA storage in GPi axon terminals, with LID triggered by enhanced GABA release into the GPi.