Elevated peripheral cytokines result in sickness and depression-like behaviors by signaling through the vagus nerve. Stimulation of the vagus nerve activates noradrenergic neurons in the nucleus of the solitary tract (NTS) and release of norepinephrine (NE) at projection sites that regulate behavior. Previous studies indicate that neurons in the locus coeruleus (LC) inhibit neurons in the NTS. This led to the hypothesis that LC neurons may act as a brake to inhibit sickness behaviors. To test this hypothesis, rats underwent baseline behavioral testing before being injected with either saline or DSP4, a neurotoxin that lesions LC neurons. Three weeks later animals underwent further behavioral testing before all animals received live E.coli injections and sickness behaviors were recorded. We expected lesioning the LC would result in greater sickness behaviors following E.coli by removing the inhibitory regulation of NTS projection neurons; however, lesioned animals had similar body weights, food intake, and sucrose intake compared to controls following E.coli challenge. Interestingly, DSP4 treated rats showed greater anxiety-like behaviors in an open field test three weeks following DPS4 and less sickness behaviors in an open field following E.coli compared to controls. The results did not support our initial hypothesis, but do support a role for LC neurons in regulating sickness and/or depression/anxiety-like behaviors. Future studies will look more into the role the LC plays in regulating behaviors and the interactions between NTS, LC, and prefrontal cortex (an area important for emotional and motivated behaviors).