Objective To explore the effect of compound rehmannia prescription on cannabinoid receptor 1 in the rats with wind syndrome due to deficiency of Yin in levodopa-induced dyskinesia (LID) in Parkinson's disease. Method A unilateral injection of 6-hydroxydopamine into the substantia nigra was performed to establish a Sprague-Dawley rat model of Parkinson's disease. The models were intraperitoneally injected with 50 mg/kg levodopa and 12.5 mg/kg benserazide for two weeks to prepare LID models with Wind syndrome due to deficiency of Yin. The models were randomly divided into LID group and compound rehmannia prescription groups. Moreover, the normal group and sham-operated group were set up, 6 rats in each group. Neurological behavior was tested after treatment for four weeks and six weeks, respectively. Then the rats were sacrificed, the brain was removed immediately and the corpus striatum was dissected out. The expression of cannabinoid receptor 1 was examined by Western blotting. Result With the prolonged time of levodopa treatment, the LID rats with wind syndrome due to deficiency of yin showed an increasing tendency of AIM scores (P<0.05), shortening of the rotation start time (P>0.05), a tendency of increased duration of continuous rotation time (P<0.01) and a reducing tendency of peak rotation rate (P>0.05). Compound rehmannia prescription improved the above mentioned neurological behavior. The expression of cannabinoid receptor 1 showed an increasing tendency in the LID groups compared with that in the normal groups. But with the prolonging time of levodopa treatment, the expression of cannabinoid receptor 1 in the LID groups showed a decreasing tendency (P<0.01). The expression of cannabinoid receptor 1 had an increasing tendency after the treatment with compound rehmannia prescription (P<0.01). Conclusions The expression of cannabinoid receptor 1 has an increasing tendency in LID rats with wind syndrome due to deficiency of yin. The changes can well reflect the severity of wind syndrome due to deficiency of yin. We would hypothesize that the treatment with compound rehmannia prescription may activate the cannabinoid receptor 1 in LID rats, inhibiting the release of excitatory amino acids, decreasing the excitability of neurons and inducing cell cascade, and finally reduce the excitatory toxicity of levodopa.