Objective Exploring the behavioral changes induced by quinpirole in obsessive-compulsive disorder (OCD) mouse, investigating the activation of neurons in different brain regions, and identifying differentially expressed genes (DEGs) and enriched biological pathways through transcriptome sequencing technology to elucidate the pathogenesis of OCD. Methods Randomly assign 32 male C57BL/6J mice, aged two months, to an OCD group and a control group (n=16). Administering quinpirole (0.75 mg/kg) via subcutaneous injection to the OCD group mice every other day for a total of 19 injections, while the control group mice received an equivalent volume of saline solution. Following the completion of the model construction, open field testing, elevated plus maze testing, and marble burying tests were conducted. After the completion of behavioral studies, tissue samples were collected. Neuronal damage was assessed using Nissl staining, while the expression of c-Fos and Iba1 proteins was examined through immunofluorescence staining. Transcriptome sequencing technology was utilized to screen for differentially expressed genes and to enrich relevant signaling pathways. The expression of inflammatory cytokines, including TNF-α, NF-κB p65, phosphorylated NF-κB p65 (p-NF-κB p65), and IL-6, was detected using Western Blot analysis. Results Mouse induced with OCD by quinpirole exhibit anxiety-like behaviors and compulsive-like behaviors. Neurons in the hippocampal and hypothalamic regions exhibit signs of damage. The expression of c-Fos and Iba1 proteins is increased in the cortex, striatum, hypothalamus, and other brain regions. Western Blot results indicate a significant increase in the expression of pro-inflammatory cytokines such as TNF-α, p-NF-κB p65, and IL-6. Conclusions In OCD mouse, neurons in multiple brain regions are abnormally activated, microglia exhibit dysfunction, and neuroinflammation induced by the activation of the NF-κB signaling pathway accompanies the development of OCD.