The more we study gut microbiota, the more it becomes evident that alterations in bacterial relative abundances are associated with aspects of human health, including cognitive function and behavior. Human studies demonstrate links between weight status, high-fat (HF) diet, and cognition; and rodent studies implicate obese- and HF diet-type microbiota in disruption of hippocampal-dependent cognition and food intake. Evidence suggests that microbiota alterations are necessary for diet-driven cognitive disruption. We do not know whether microbiota changes alone are sufficient to induce these deficits. This thesis will first discuss mechanisms through which microbiota modulates food intake and cognition. Then, I will describe a study in which rats were given an antibiotic cocktail and recolonized with chow- or HF-type microbiota. We then assessed learning and memory function, neuroinflammation, and brain insulin signaling. We found that HF-type microbiota colonization is sufficient to induce neuroinflammation and alter insulin receptor gene expression and hippocampal-dependent cognition.
