The Section of Neurobiology

Research Topics

1. Systems neuroscience
2. Neural control of metabolism
3. Ingestive behaviors

Research Overview

Our 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.

Selected Publications

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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., Sanchez-Watts, G., Liu, Y. and Aguilera, G. (2011) The Distribution of messenger RNAs encoding the three isoforms of the Transducer Of Regulated CREB Activity (TORC) in the rat forebrain. J.Neuroendocrinology 23: 754-766. -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

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Boyle CN, & Watts AG. (2010) The functional architecture of dehydration-anorexia. Physiology & Behavior. 100: 472-477. -PubMed

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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