Alan G. Watts
Department of Biological Sciences
Phone: (213) 740-1497
University of Southern California
Hedco Neuroscience Building, Rm 416
3641 Watt Way
Los Angeles, CA 90089
- BSc (Hons): University of Wales, UK
- D.Phil: University of Oxford, UK
- Post-Doc: Salk Institute, La Jolla, CA
- Systems neuroscience
- Neural control of metabolism
- Ingestive behaviors
Research OverviewOur work is directed towards understanding how the brain contributes to the development, manifestation, and complications of diabetes and obesity. We do this in two projects that focus on the neural control of energy metabolism.
The first project investigates how peripheral metabolism interacts with the brain to generate adrenocortical and sympathoadrenal hormonal responses. In particular, we are interested in the way that two critical metabolic signals--glucocorticoid hormones and blood glucose (glycemia)--are sensed by the brain, and then generate appropriate counter-regulatory responses.
How the brain and the body senses changes in blood glucose is a fundamental physiological process, the understanding of which is critical to the etiolology of both forms of diabetes. We are interested in how glucocorticoids and neurotransmitters interact with neurons in the hypothalamus, which is a major integrative locus for metabolic control. A major focus of our work is on sets of hindbrain catecholaminergic neurons that project to the forebrain. These neurons are crucial for detecting and encoding information about blood glucose levels. We investigate the way that catecholaminergic neurons and glucocorticoids affect signal transduction and gene regulatory mechanisms in sets of forebrain neurons responsible for regulating metabolism in health and disease.
This work is highlighted in a recent USC News story:
USC Scientists Find Missing Link in Regulation of Glucose
The second project investigates the neural basis of anorexia using dehydration as a physiological challenge. The goal here is to understand the structure and functional interactions between the neural systems that inhibit and stimulate feeding, particularly between the cortex, hypothalamus, and hindbrain.
The techniques we use include: whole animal physiology, in situ hybridization, immunocytochemistry (with confocal and conventional immunofluorescence), tract-tracing, behavioral analysis, and neuroinfomatics.
Kaminski, K & Watts, A.G. (2012) Intact catecholamine inputs to the forebrain are required for appropriate regulation of CRH and vasopressin gene expression by corticosterone in the rat paraventricular nucleus. J. Neuroendocrinology 24: 1517-1526. -PubMed
Liu, Y., Poon, V., Sanchez-Watts, G., Watts, A.G., Takemori, H. & Aguilera, G. (2012) Salt inducible kinase is involved in the regulation of corticotropin releasing hormone transcription in hypothalamic neurons in rats. Endocrinology 153: 223-233. -PubMed
Khan, A.M., Kaminski, K.L., Sanchez-Watts, G., Ponzio T.A., Kuzmiski, J.B., Bains, J.S., & Watts, A.G. (2011) MAP kinases couple hindbrain-derived catecholamine signals to hypothalamic adrenocortical control mechanisms during glycemia-related challenges. J. Neuroscience 31: 18479-18491. -PubMed
Watts A.G. (2011) Structure and function in the conceptual development of mammalian neuroendocrinology between 1920 and 1965. Brain Research Reviews 66: 174-204. -PubMed
Boyle CN, Lorenzen SM, Compton D, Watts AG. (2011) Dehydration-anorexia derives from a reduction in meal size, but not meal number. Physiology & Behavior. 105: 305-14. (Epub 2011 Aug 11.) -PubMed
Boyle CN, & Watts AG. (2010) The functional architecture of dehydration-anorexia. Physiology & Behavior. 100: 472-477. -PubMed
Khan, A.M., Ponzio, T.A., Sanchez-Watts, G., Stanley, B.G., Hatton, G.I. & Watts, A.G. (2007) Catecholaminergic control of MAP kinase signaling in paraventricular neuroendocrine neurons in vivo and in vitro: A proposed role during glycemic challenges. J. Neuroscience 27: 7344-7360. -PubMed