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Overconsumption of highly palatable "junk food" contributes to obesity and related metabolic disorders. This project investigated the brain circuitry that allows such eating in excess of the body's energy requirements. We hypothesized that neurotransmitters mediating energy homeostasis and food reward interact within the nucleus accumbens (NAc) to control the intake of palatable foods. Specifically, we examined two neuronal projections from the hindbrain to the NAc: glucagon-like peptide 1 (GLP-1) and the A2 population of noradrenergic (NA) neurons. Both GLP-1 and A2 cell bodies are located in the nucleus of the solitary tract (NTS) and receive input from the gastrointestinal tract about incoming nutrients during meals. Our lab has previously shown that GLP-1 can act within the NAc to reduce feeding, but that maintenance on high-fat diet (HFD) impairs this response. We hypothesized that this impairment is caused by endogenous opioid activation of mu-opioid receptors (MOR) in NAc. Our studies further examined the HFD-induced impairment in GLP-1 sensitivity and attempted to lay the groundwork for investigating a possible interaction between GLP-1 and MOR in NAc. The next series of studies focused on the role of the A2 projection to NAc. We had previously found that selective lesion of this projection caused overeating and weight gain. Here we asked whether this lesion affects energy expenditure or locomotor activity. We did not observe any significant effects, but also failed to replicate the body weight effect previously obtained, so the data are not conclusive. Further analysis is ongoing.
