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Abstract
Diet-induced obesity in rodent models is associated with brain pathophysiologies including impaired hippocampal-dependent memory and anxiety-like behavior. Dietary patterns associated with obesity lead to deleterious changes in gut microbiota composition (gut dysbiosis) and chronic low-grade inflammation. These changes may mediate the impact of obesity on behavior by increasing neuroinflammation. Here we discuss the evidence for diet- and microbiota-related impairments in hippocampal memory and describe potential mechanisms with an emphasis on the vagus nerve and systemic inflammation. One contributor to systemic inflammation is the bacterial compound lipopolysaccharide (LPS), which increases in states of obesity and dysbiosis and leads to chronic low-grade inflammation. We tested the impact of chronic LPS infusions on neuroinflammation, anxiety, and memory in rats. We found that chronic low-dose LPS increased neuroinflammation in select brain areas, altered stress hormone levels, decreased anxiety-like behavior, and had no impact on hippocampal memory function.