Inflammatory bowel disease (IBD) is characterized by chronic inflammation and significantly impairs quality of life through anxiety-like behaviors and visceral pain. Early evaluation of the risk of anxiety-like behaviors and visceral pain in IBD patients, along with targeted treatment, may benefit disease management. Visceral pain and anxiety-like behavior are often accompanied by neurological damage. Previous studies have shown that abnormal accumulation of glutamate can cause excitatory neurotoxic effects, leading to central nervous system (CNS) damage. Excitatory amino acid transporters (EAATs), particularly EAAT2, are known to regulate glutamate levels. The impact of hippocampal EAAT2 modulation on these clinical features in IBD is yet to be evaluated. Therefore, we designed this experiment to test this hypothesis. This study aimed to investigate the impact of altered levels of hippocampal EAAT2 on anxiety-like behaviors and visceral pain in mice with IBD. We observed reduced EAAT2 expression, increased glutamate levels, elevated N-methyl-d-aspartate receptors (NMDAR) expression, and obvious glutamate toxicity in the hippocampus of dextran sulfate sodium (DSS) induced IBD model mice. These mice exhibited significant visceral pain and anxiety-like behaviors. In summary, the reduced expression of EAAT2 in the hippocampus of individuals with IBD leads to elevated glutamate levels, resulting in neuronal damage and ultimately contributing to visceral pain and anxiety-like behaviors. These findings suggest that EAAT2 could serve as a therapeutic target for neurologically derived IBD symptoms.