Abnormal dopamine signaling in the striatum is associated with compulsive behaviors including behavioral repetition; however, the molecular mechanisms remain unclear. Here, we demonstrated that a superoxide-producing enzyme, NOX1/NADPH oxidase regulated repetitive behaviors in mice through facilitating excitatory synaptic inputs in the central striatum (CS). Repeated stimulation of D₂ receptors induced compulsive-like repetitive behaviors, which were significantly ameliorated by Nox1 deficiency or pharmacological inhibition of NOX1. Nox1 mRNA was highly expressed in the striatum and repeated D₂ receptor stimulation further upregulated Nox1 expression in the CS. Repeated D₂ receptor stimulation facilitated excitatory inputs in CS indirect pathway medium spiny neurons (iMSNs) and this effect was suppressed by the genetic deletion or pharmacological inhibition of NOX1. Nox1 deficiency potentiated protein tyrosine phosphatase activity and attenuated the accumulation of activated Src kinase which was required for synaptic potentiation in CS iMSNs. NOX1 inhibition or neuron-specific knockdown of Nox1 in the CS was sufficient to ameliorate repetitive behaviors. Collectively, these results indicate that NOX1 acts as an enhancer of synaptic facilitation in CS iMSNs and plays a key role in the molecular link between abnormal dopamine signaling and behavioral repetition.