The vast amount of gut microbiota demonstrates the ability to modulate brain function. Unlike the brain, the gut microbiota is highly accessible to direct interventions such as prebiotics, probiotics and antibiotics, and can be manipulated by lifestyle choices including diet. The dendrites of neurons are the main input compartment, and proper dendritic growth and arborization are critical for the proper functioning of the central nervous system. Most studies of dendritic growth have shown that the dendritic growth process is extremely dynamic. Although there is some evidence that the gut microbiome can influence neuronal dendritic morphology, several studies are needed to unravel the effect of the gut microbiome in many brain areas. The establishment of distinct representations and memories of multiple contexts and episodes is thought to be a critical function of the hippocampal-entorhinal cortical network. Whether the gut microbiome can influence the dendritic growth of entorhinal inhibitory interneurons remained unexplored. Therefore, adult GAD67-GFP mice were used for the experiments. Mice in the antibiotic-treated group received a cocktail of antibiotics: Vancomycin, Meropenem, Neomycin and Clindamycin daily for 3 weeks. Using this mouse model, we investigated whether antibiotic-induced dysbiosis affects the morphology of GABAergic inhibitory interneurons in the brain. We quantified the dendritic morphology of GAD67-positive interneurons in the antibiotic-induced dysbiosis group compared to the control group. Our results showed that antibiotic-induced dysbiosis can reduce dendritic morphology of GAD67-positive interneurons. These results suggest a role for the gut microbiome in regulating the dendritic morphology of inhibitory interneurons.