Electroconvulsive therapy (ECT) is a well-established treatment for psychiatric disorders. Recent reports show that ECT improves motor deficits in Parkinson's disease (PD), while the mechanism of action remains unclear. To investigate the effects of ECT in PD, we produced partial dopaminergic depletion by unilateral striatal injection of 6-OHDA. After three weeks, behavioral testing was performed using the open field and corridor test. Animals with a lateralized phenotype were randomized into ECT or sham treatment. After a two-week treatment interval with daily ECT, behavioral testing was repeated. We found a significant increase in general locomotor activity (distance traveled in the open field after ECT +34.5% IQR [11-61%] vs. sham -10.8 % IQR [-19-15%]) and attenuation of the lateralized motor phenotype (sugar pellet retrievals in the corridor test from the lesioned body site after ECT +139% IQR [42-220%] vs. sham +27% IQR [-42-79%] following ECT. Immunolabeling of the dorsal striatum with tyrosine hydroxylase (TH) one week after the last treatment revealed a partial recovery of dopaminergic axon denervation in ECT vs. sham (area covered by TH+ fibers increased by 149.1±25.9% normalized to the average of the sham group, p=.0001, t-test). In addition, we examined postsynaptic neuroplasticity by electrophysiological analysis of striatal spiny projection neurons (SPNs) and found that ECT partially normalized the 6-OHDA-induced hyperexcitability in D1-SPNs. In summary, our data suggests that ECT causes dopamine axonal reinnervation in a mouse model of late-stage PD, providing a basis for future clinical studies.