Depressive disorders occur in 40%–50% of patients with Parkinson’s disease. Calcitonin gene-related peptide (CGRP) is a neuropeptide known as a pain transmitter. Our previous study suggested that intracerebroventricular administration of CGRP improves depressive-like behaviors. Here, we presented evidence that CGRP-deficient knockout (CGRP KO) mice exhibit Parkinson’s disease symptoms with depression-like behaviors. We also investigated whether intranasal administration of CGRP affects the amelioration of Parkinson’s disease-like symptoms in CGRP KO mice. Saline or CGRP (0.1 mM) was intranasally administered to 10-week-old CGRP KO mice for 2 weeks. We performed several behavioral paradigm tests to evaluate the mice’s motor and cognitive functions: open field, catalepsy, pole, rotarod, hind-limb, and adhesive removal. Motor dysfunction was observed in the CGRP KO mice in all behavioral tests compared with the wild-type control C57BL6/J mice. Intranasal administration of CGRP ameliorated motor function in the rotarod test and tended to improve it in the catalepsy test. This administration also increased the level of tyrosine hydroxylase in the substantia nigra in the CGRP KO mice. This study’s results suggest that CGRP replacement is a novel therapeutic approach for Parkinson’s disease.