个人简介

Ph.D. Northwestern University Neurobiology & Behavior Group Cellular, Molecular Biology and Physiology Group Neurobiology of Feeding and Food Reward

研究领域

The main interest of my laboratory is the neural regulation of feeding and body weight, including the development of obesity. We focus primarily on the mesolimbic dopamine system, which is the brain’s “reward” circuitry. While these neural “reward” circuits are primarily associated with their roles in drug abuse and addiction, it has been suggested that they were originally designed to respond to natural rewards such as food and water. For example, multiple studies have shown that food can act as a “reward” to stimulate dopamine release in specific regions of the brain similar to what is seen with abused drugs. The rise in obesity levels has been paralleled by a significant increase in the intake of processed foods high in fat and sugar, suggesting that pathways regulating the intake of these foods may be sites that could be targeted for therapies to help prevent or reverse obesity. Thus, we are interested in how pleasurable & appetizing foods (such as those high in fat and sugar) activate the “reward” pathways in the brain, and how these responses change with obesity. In addition, we are trying to understand how changes in the activity of dopamine pathways in turn affect feeding and body weight. In the lab we use a number of different techniques to examine these questions, including cellular electrophysiology and immunohistochemistry, along with multiple different cellular, molecular and genetic approaches.

How does feeding affect the activity of different parts of the mesolimbic dopamine system? In these studies we are trying to determine how feeding affects the activity of different components of dopamine circuitry, and how these changes affect other processes such as future feeding and drug abuse/addiction. For example, we are seeking to understand the changes that occur when animals are allowed restricted or prolonged access to appetizing high fat or high sugar foods, or when they undergo feeding protocols similar to what is seen with human dieting. How do other hormones, neurotransmitters and neuropeptides interact with dopamine circuitry to regulate feeding and body weight? There are a large number of substances that play an important role in the regulation of feeding and body weight, and many of them have been shown to interact with dopamine pathways (i.e. leptin, insulin, ghrelin, orexin etc). We are currently focusing on a family of peptides termed the melanocortins. These are peptides that are expressing the hypothalamus and serve to decrease feeding, stimulate energy expenditure, and regulate glucose levels. We are using a number of different techniques to determine whether melanocortins regulate processes such as feeding, activity, and drug abuse/addiction through actions on the mesolimbic dopamine system. Development of tools to activate or inhibit specific populations of neurons. We are also currently developing tools (employing the light activated channels Channelrhodopsin and Halorhodopsin and the Designer Receptors Exclusively Activated by a Designer Drug [DREADD]) with the goal of being able to activate or inhibit distinct, specific populations of neurons in the brain. This will allow us to examine the roles of specific neuronal populations in the regulation of a variety of behaviors ranging from feeding to drug abuse.

近期论文

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Neuropeptide-Y alters VTA dopamine neuron activity through both pre- and post-synaptic mechanisms. West KS, Roseberry AG. J Neurophysiol. 2017 May 3:jn.00879.2016. doi: 10.1152/jn.00879.2016. [Epub ahead of print] Altered sucrose self-administration following injection of melanocortin receptor agonists and antagonists into the ventral tegmental area. Shanmugarajah L, Dunigan AI, Frantz KJ, Roseberry AG. Psychopharmacology (Berl). 2017 Jun;234(11):1683-1692. doi: 10.1007/s00213-017-4570-4. Epub 2017 Feb 27. Neurotensin inhibits both dopamine- and GABA-mediated inhibition of ventral tegmental area dopamine neurons. Stuhrman K, Roseberry AG. J Neurophysiol. 2015 Sep;114(3):1734-45. doi: 10.1152/jn.00279.2015. Epub 2015 Jul 15. Regulation of the mesocorticolimbic and mesostriatal dopamine systems by α-melanocyte stimulating hormone and agouti-related protein. Roseberry AG, Stuhrman K, Dunigan AI. Neurosci Biobehav Rev. 2015 Sep;56:15-25. doi: 10.1016/j.neubiorev.2015.06.020. Epub 2015 Jun 24. Review. Acute fasting increases somatodendritic dopamine release in the ventral tegmental area. Roseberry AG. J Neurophysiol. 2015 Aug;114(2):1072-82. doi: 10.1152/jn.01008.2014. Epub 2015 Jun 17. Decreased consumption of rewarding sucrose solutions after injection of melanocortins into the ventral tegmental area of rats. Yen HH, Roseberry AG. Psychopharmacology (Berl). 2015 Jan;232(1):285-94. doi: 10.1007/s00213-014-3663-6. Epub 2014 Jul 3. Altered feeding and body weight following melanocortin administration to the ventral tegmental area in adult rats. Roseberry AG. Psychopharmacology (Berl). 2013 Mar;226(1):25-34. doi: 10.1007/s00213-012-2879-6. Epub 2012 Sep 26. Decreased vesicular somatodendritic dopamine stores in leptin-deficient mice. Roseberry AG, Painter T, Mark GP, Williams JT. J Neurosci. 2007 Jun 27;27(26):7021-7.