Exercise decreases aberrant corticostriatal plasticity in an animal model of L-DOPA-induced dyskinesia

Physical exercise attenuates the development of L-DOPA-induced dyskinesia (LID) in 6-hydroxydopamine-induced hemiparkinsonian mice through unknown mechanisms. We now tested if exercise normalizes the aberrant corticostriatal neuroplasticity associated with experimental murine models of LID. C57BL/6 mice received two unilateral intrastriatal injections of 6-hydroxydopamine (12 μg) and were treated after three weeks with L-DOPA/benserazide (25/12.5 mg/kg) for four weeks, with individualized moderate-intensity running (60-70% V̇O2peak) or not (untrained). L-DOPA converted the pattern of plasticity in corticostriatal synapses from a long-term depression (LTD) into a long-term potentiation (LTP). Exercise reduced LID severity and decreased aberrant LTP. These results suggest that exercise attenuates abnormal corticostriatal plasticity to decrease LID.