Inflammatory bowel diseases (IBD) affect the gastrointestinal tract and can lead to extra-gut effects, including depression and anxiety related to the brain. Specifically, certain brain regions, such as the hippocampus, respond to bowel inflammation by modulating neuronal and glial activity. During the peak of inflammation, hippocampal regions undergo changes in glial properties that are associated with alterations in excitatory synaptic transmission. Additionally, bowel inflammation compromises the integrity of the blood-brain barrier, leading to the infiltration of immune cells and metabolites.The aim of this study is to elucidate the cellular and molecular mechanisms underlying the observed alterations in the central nervous system. To achieve this goal, we utilized a mouse model of acute intestinal inflammation induced by 2,4-Dinitrobenzenesulfonic acid hydrate (DNBS). We conducted electrophysiological recordings of spontaneous and evoked glutamatergic and GABAergic transmission in hippocampal slices to assess the effects of peripheral inflammation on synaptic functionality. Our findings reveal dysfunctional synaptic transmission in the DNBS model. Furthermore, to investigate the mechanisms underlying the observed synaptic alterations, we analyzed the morphology and density of glial cells. Our results indicate that peripheral inflammation induces gliosis, particularly an increase in microglia and astrocyte densities in the hippocampus. Additionally, we are assessing changes in gut metabolites that could potentially mediate hippocampal alterations resulting from peripheral inflammation.In conclusion, our study demonstrates that peripheral inflammation induces gliosis, leading to alterations in synaptic functionality in the hippocampus.