Abstract: Objective To explore the specific molecular mechanism of postsynaptic NK1 receptor involved in Parkinson’s disease (PD) with motor complications, and to provide a new method and target for the treatment of levodopa-induced dyskinesia (LID). Methods A mice model of PD was induced by stereotaxically injection of 6-hydroxydopamine into the left striatum, the successful PD model was randomly divided into four groups and each groups was treated with different dose of NK1 antagonist or vehicle. At the same time, a group of sham-operated mice were involved as control. The mice in sham-operated group, PD group and LID group were intrastriatally given vehicle. After half an hour, mice in LID group and NK1 receptor antagonist group were administrated levodopa (15mg/kg, i.p.) plus benserazide (12mg/kg, i.p.). Mice in sham group and PD group were given vehicle. Behavior observation was used to observe the effect of NK1 antagonist on abnormal involuntary movement (AIM). Western-blot was used to detect the phosphorylated levels of DARPP-32, ERK, GluR1 and NR1 in the striatum of mice. Results The AIM scores were increased after levodopa priming. But the AIM scores were decreased after given medium concentration NK1 receptor antagonist (0.05 nmol/μL) (P <0.01). But low and high concentration NK1 receptor antagonist had no effect on AIM scores. Western blot results indicated that the phosphorylation levels of DARPP32, ERK1/2, GluR1 and NR1 of mice in PD group were significantly lower than those in sham group (all P <0.01)，But these molecules were significantly increased after levodopa priming (P <0.01). By contrast, coadministration of NK1 antagonist (0.05 nmol/μL) and levodopa suppressed the increase of these phosphorylated protein expression in PD mice (P<0.05). Conclusion NK1 receptor antagonist could reduce the incidence of LID in PD mice，postsynaptic NK1 receptor was involved in the development of LID.