Faculty Profile

Steven R. Vigna, Ph.D. (Zoology, University of Washington) Associate Professor, Department of Cell Biology, Division of Physiology Associate Professor, Department of Medicine, Division of Gastroenterology Programs: CMB, Cancer Center, Gastroenterology Training Grant	We are interested in the mechanisms of signal transduction of neuropeptides and peptide hormones, mechanisms of receptor regulation, and the role of receptor regulation in health and disease. The major peptide of interest is the neurotransmitter substance P which is involved in gastrointestinal tract regulation, pain pathways, inflammation, and central nervous system functions. Our major focus is at the level of the receptors for this peptide. We are currently studying mechanisms of substance P receptor desensitization, resensitization, and downregulation in model cell systems and using analysis of substance P-induced endocytosis of the substance P receptor to reveal mechanisms of pain transmission and inflammation in vivo in animal models. The approaches used to investigate questions of interest are pharmacological, cellular, biochemical, and molecular.

E-mail srv@duke.edu V.A. Medical Center, Room A2028 Box 3709, Duke University Medical Center Durham, NC 27710 Telephone 919-286-0411 ext. 7293 Fax 919-286-5530

Selected Publications
Vigna, S. R. 2003. The role of the amino-terminal domain of tachykinins in neurokinin-1 receptor signaling and desensitization, Neuropeptides 37, 30-35.

McVey, D. C., Schmid, P. C., Schmid, H. H. O., and Vigna, S. R. 2003. Endocannabinoids induce ileitis in rats via the capsaicin receptor (VR1), J. Pharmacol. Exp. Therap. 304, 713-722.

Nathan, J.D., Peng, R.Y., Wang, Y., McVey, D.C., Vigna, S.R., and Liddle, R.A. 2002. Primary sensory neurons: a common final pathway for inflammation in experimental pancreatitis in rats, Am. J. Physiol. 283, G938-G946.

Nathan, J.D., Patel, A. A., McVey, D.C., Thomas, J. E., Prpic, V., Vigna, S. R., and Liddle, R. A. 2001. Capsaicin vanilloid receptor-1 mediates substance P release in experimental pancreatitis, Am. J. Physiol. 281, G1322-G1328.

McVey, D. C., and Vigna, S. R. 2001. The capsaicin VR1 receptor mediates substance P release in toxin A-induced enteritis in rats, Peptides 22, 1439-1446.

Vigna, S.R. 2001. The N-terminal domain of substance P is required for complete homologous desensitization but not phosphorylation of the neurokinin-1 receptor, Neuropeptides 35, 24-31.

Mantyh, C. R., Mc,Vey, D. C., and Vigna, S. R. 2000. Extrinsic surgical denervation inhibits Clostridium difficile toxin A-induced enteritis in rats, Neurosci. Lett. 292, 95-98.

Vigna, S. R. 1999. Phosphorylation and desensitization of the neurokinin-1 receptor expressed in epithelial cells. J. Neurochem. 73: 1925-1932.

Current Projects
Chris Mantyh (Collaborator): The role of substance P in intestinal inflammation.

Douglas McVey (Technician): The role of the capsaicin VR1 receptor in intestinal inflammation; Mechanisms of substance P activation of MAP Kinase.

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