A previous study observed oxytocin‐induced enhancement of sIPSC in SNc DA neurons, but no significant change in sIPSC was detected in our study, which may be due to the high chloride internal solution used to amplify sIPSC.[23] In the MPTP‐induced PD model, consistent with previous studies showing that acute MPTP application elevated excitatory synaptic transmission via presynaptic mechanisms,[60, 61] we observed the elevation of excitatory synaptic inputs to SNc DA neurons (Figure 7), which was reversed by exogenous oxytocin application. The gene discussed is OXT; the disease is Parkinson disease.