HTR1A and drug-induced dyskinesia: Given that aberrant facilitation of corticostriatal synaptic transmission is considered a major contributor to L-DOPA-induced dyskinesia (reviewed in [94]), moderating cortical neuronal activity, or glutamate release from corticostriatal terminals via 5-HT1A receptors located on these terminals [44], could be additional mechanisms underlying the vilazodone effects on dyskinesia.