Research in the Davis lab is focused on detailing the impact of neuroendocrine signaling on dopamine release and reward-based behaviors. In this capacity, there are two main focuses of the lab: 1) determine the ability of feeding peptides to regulate palatable food, ethanol and psychostimulant reward through action in mesolimbic circuits and 2) evaluating change in addictive behaviors following weight loss surgery.
In general, work from our lab has demonstrated that feeding peptides that stimulate food intake like ghrelin, melanocortin peptides and orexin also augment the motivation to obtain palatable food through acting in mesolimbic circuits which stimulate forebrain dopamine release. In contrast, factors that inhibit food intake like the adipocyte derived hormone leptin decrease the motivation to obtain palatable food and attenuate dopamine release through action in mesolimbic centers. Our recent work has focused on the brain arousal peptide orexin which is released upon exposure to cues linked to the receipt of palatable food. In turn, orexin stimulates brain dopamine release, food seeking behavior and hedonic feeding. We found that orexin is capable of acting in the paraventricular thalamic nucleus (PVT), a key relay center linking the hypothalamus to limbic structures in the forebrain. Thus orexin signaling has gained prominence as a key system capable of integrating neuroendocrine signals from hypothalamic brain regions with regions that regulate brain dopamine to control behavior(s) that ultimately influence motivation to obtain food rewards.
A separate area of study in the lab is focused on understanding how weight loss surgery induces dramatic changes in addictive-type behaviors. In terms of obesity, weight loss surgery is the only reliable way to produce significant decreases in body weight that are sustained throughout time. The Roux en Y Gastric Bypass Surgery (RYGB) is a common form of weight loss surgery that limits the size of the stomach and re-routes the intestines. Apart from dramatic decreases in body weight, RYGB leads to substantial increases in neuroendocrine hormones that regulate brain reward and addictive behavior(s). For example, RYGB increases sensitivity to alcohol. In particular, RYGB stimulates alcohol intake in individuals that typically refrain from drinking, whereas it decreases alcohol intake and craving in alcoholics. More recent work in this area indicates that RYGB also increases sensitivity to psychostimulant drugs of abuse. Mechanistic studies on this topic indicate that post-surgical changes in ghrelin, orexin and the gut peptide glucagon-like peptide-1 (GLP-1) play a permissive role regulating the increased sensitivity to ethanol following RYGB. A current goal of the lab is to determine the mechanisms that regulate increased sensitivity to psychostimulant drugs following RYGB.
Jon Davis, Assistant Professor in IPN, received his B.S. in Biology from Maryville College, Maryville, Tennessee in 1997. He then received a PhD in 2005 from the University of Cincinnati College of Medicine, Department of Cell Biology & Anatomy, Cincinnati, Ohio. From 2005-2010 he did postdoctoral work at the University of Cincinnati within the Obesity Research Center. He then went on to become a Research Scientist within the Department of Psychiatry & Behavioral Neuroscience at University of Cincinnati. In 2014, he was appointed to the faculty as an Assistant Professor at Washington State University, Pullman, WA, USA.