Jessica Barson
Jessica Barson is an American neuroscientist and associate professor at Drexel University College of Medicine. Barson investigates neuropeptide signalling in the paraventricular nucleus of the thalamus as well as the nucleus accumbens to understand the neurobiological basis of addiction and elucidate targets for therapy. Early life and education. From an early age Barson was interested in the brain. She decided to pursue her undergraduate studies in psychology at Columbia College, Columbia University. During her time at Columbia, Barson worked in the lab of Geraldine Downey as a research assistant studying social psychology and developmental psychopathology. During the later  part of her time at Columbia, Barson worked in the lab of Jon Horvitz studying the neurobiological basis of learning and memory. Barson obtained her B.A. and graduated summa cum laude from Columbia in 2000 as a member of the Phi Beta Kappa honors society. After her research experiences at Columbia, Barson pursued a Post-Baccalaureate Pre-Medical Program at Columbia, where she continued to work in research as a technician and research assistant at the New York State Psychiatric Institute until 2003. Continuing on an academic path, Barson pursued her master's degree and graduate research in neuroscience and  psychology at Princeton University in 2004. She trained under the mentorship of Bart G. Hoebel studying the regulation of alcohol intake by dietary fat and fat-stimulated neuropeptides. In 2006, Barson obtained her Master of Arts in Psychology and Neuroscience, and then in 2009, Barson obtained her PhD in Psychology and Neuroscience. Following her graduate training, Barson moved to New York City to complete her postdoctoral research training at The Rockefeller University in Behavioral Neurobiology in 2009. Barson worked under the mentorship of Sarah Fryer Leibowitz continuing to study the role of opioids and orexin in ethanol consumption and feeding . Barson completed her postdoctoral studies in 2014. Alcohol Consumption and Dietary Fat Intake. During graduate school, Barson explored the relationship between alcohol consumption and fat metabolism to understand how the mechanisms that control reward or food intake may also regulate alcohol consumption. There exists a positive behavioral feedback loop with fat consumption such that fat intake leads to increased consummatory behavior due to orexin and opioid release in the brain. In her work, Barson probed the mechanisms of this positive feedback loop at play during alcohol consumption. She found that ethanol could substitute for fat in this positive feedback loop  that decreasing circulating lipid levels leads to decreased ethanol intake. Barson explored this fascinating interconnectivity between fat and ethanol metabolism and their impacts on behavior. Barson found that ethanol increases the same fat-stimulated neuropeptides, orexin and opioids, in the brain and the more ethanol they voluntarily consume, the higher the expression level of these neuropeptides. Further she found that decreases in ethanol consumption, decrease expression of orexin. Probing the effects of opioids on consummatory behavior, Barson injected opioids into brain regions involved in feeding and reward and found increases in alcohol consumption and increases in dopaminergic release in the  nucleus accumbens, typically involved in reward behavior. Barson's work highlighted novel mechanisms driving alcohol intake which create future opportunities for development of targeted strategies to prevent alcohol abuse. In Barson's first author paper published in the journal Alcohol, Barson shows a strategy to intervene the vicious cycle between fat and alcohol, where consumption of the two synergistically act to drive brain processes that drive further consumption. Since both fat and alcohol appear to increase blood triglyceride levels, Barson administered a triglyceride lowering drug called Gemfibrozil which caused a significant reduction in orexigenic peptide and reduced ethanol intake. Neural  Basis of Feeding and Reward. During her postdoctoral studies at Rockefeller, Barson continued to follow up on her graduate work, exploring mechanistically the regulation of neuropeptides in the regulation of addiction and food consumption. Since previous studies showed that, just like the opioid enkephalin, galanin and orexin are also stimulated by dietary fats. Following up on this knowledge, Barson and her team explored which areas of the hypothalamic paraventricular nucleus (PVN) are specifically stimulated by high fat diets as well as exploring whether the ligands or receptors for galanin and orexin are over-expressed in these areas. Interestingly, Barson found  strong overlap in galanin expressing cells and enkephalin expressing cells in the medial PVN of rats fed a high fat diet but not rats fed normal chow. Further, they found the same pattern in co-expression of orexin receptor 2 and enkephalin after high fat diet in a region immediately posterior to the medial PVN. These findings show how non-opioid peptides might be interacting with opioid signalling in high fat diets to mediate increased consummatory behavior. In addition to her work exploring the neurochemical mechanisms of consummatory behavior, Barson also explored how individual variability can account for differences in  consummatory behavior. Since alcoholism, and other addictive disorders, show significant variability in both propensity towards addiction and effects of treatments, it is essential to probe the underlying biology of these differences in order to better treat addiction in the fashion of personalized medicine. They first identified subgroups of ethanol naive rats based on two measures known to predispose individuals to high ethanol consumption; high novelty-induced activity and high-fat-induced triglycerides. Barson and her colleagues then trained them to drink ethanol and observed that high activity rats had both increased alcohol intake as well as increased levels of galanin  and enkephalin in the PVN as well as increased orexin in the perifornical lateral hypothalamus (PFLH). In the high triglyceride rats, they greater expression in the PVN but reduced orexin in the PFLH showing that while the two predicted high ethanol consumption groups exhibited high alcohol consumption, the endogenous peptide and drug responses markedly differed. Career and research. Barson worked for one year as a research associate in the lab of Leibowitz, but by 2015 Barson was recruited to Drexel University College of Medicine to become an assistant professor and start her own lab in the Department of Neurobiology and  Anatomy. Barson was simultaneously promoted to Adjunct Faculty at The Rockefeller University in 2015, a position she held until 2017 while starting her lab at Drexel. At Drexel, Barson's research program is centered around studying the neural basis of addiction, with a focus on neuropeptidergic actions within the limbic system and their specific role in alcohol disorder and binge eating disorder. In addition to conducting research and teaching, Barson is an editor for "Frontiers in Systems Neuroscience", "Frontiers in Neuroscience", and previously "Frontiers in Psychology". She is also a guest editor for "Frontiers in Behavioral Neuroscience and Brain Research