Gαolf mutation allows parsing the role of cAMP-dependent and extracellular signal-regulated kinase-dependent signaling in l-3,4-dihydroxyphenylalanine-induced dyskinesia
Although l-3,4-dihydroxyphenylalanine (l-DOPA) remains the reference treatment of Parkinson's disease, its long-term beneficial effects are hindered by l-DOPA-induced dyskinesia (LID). In the dopamine (DA)-denervated striatum, l-DOPA activates DA D1 receptor (D1R) signaling, including cAMP-dependent protein kinase A (PKA) and extracellular signal-regulated kinase (ERK), two responses associated wi