Steven R. Vigna, PhD

Associate Professor of Cell Biology
Associate Professor in Medicine
Campus mail Duke Box 103859, Durham, NC 27710
Phone (919) 684-8860
Email address steven.vigna@duke.edu

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.

Education and Training

  • Ph.D., University of Washington, 1978
  • B.S., University of Washington, 1971

Publications

Nathan, JD, Peng, RY, Wang, Y, McVey, DC, Vigna, SR, and Liddle, RA. "Primary sensory neurons: A common final pathway for inflammation in experimental pancreatitis in rats." American Journal of Physiology Gastrointestinal and Liver Physiology 283, no. 4 46-4 (October 1, 2002).

Scholars@Duke

Nathan, JD, Patel, AA, McVey, DC, Thomas, JE, Prpic, V, Vigna, SR, and Liddle, RA. "Capsaicin vanilloid receptor-1 mediates substance P release in experimental pancreatitis." American Journal of Physiology Gastrointestinal and Liver Physiology 281, no. 5 44-5 (December 18, 2001).

Scholars@Duke

Nathan, JD, Patel, AA, McVey, DC, Thomas, JE, Prpic, V, Vigna, SR, and Liddle, RA. "Capsaicin vanilloid receptor-1 mediates substance P release in experimental pancreatitis." American Journal of Physiology. Gastrointestinal and Liver Physiology 281, no. 5 (November 2001): G1322-G1328.

PMID
11668042
Full Text

McVey, DC, and Vigna, SR. "The capsaicin VR1 receptor mediates substance P release in toxin A-induced enteritis in rats." Peptides 22, no. 9 (September 2001): 1439-1446.

PMID
11514026
Full Text

Nathan, JD, McVey, DC, Patel, A, Thomas, J, Vigna, SR, and Liddle, RA. "Vanilloid receptor-1-mediated substance P release in experimental pancreatittis in mice." Gastroenterology 120, no. 5 (April 2001): A539-A539.

Full Text

Vigna, SR. "The N-terminal domain of substance P is required for complete homologous desensitization but not phosphorylation of the rat neurokinin-1 receptor." Neuropeptides 35, no. 1 (February 2001): 24-31.

PMID
11346307
Full Text

Mantyh, CR, McVey, DC, and Vigna, SR. "Extrinsic surgical denervation inhibits Clostridium difficile toxin A-induced enteritis in rats." Neurosci Lett 292, no. 2 (October 6, 2000): 95-98.

PMID
10998557
Scholars@Duke

Patel, AA, Thomas, JE, McVey, DC, Prpic, V, Vigna, SR, and Liddle, RA. "The capsaicin vanilloid receptor-1 (VR-1) mediates a portion of secretagogue-induced pancreatitis in mice." Gastroenterology 118, no. 4 (April 2000): A169-A169.

Full Text

Mantyh, CR, McVey, DC, and Vigna, SR. "Extrinsic denervation inhibits clostridium difficile toxin A-induced enteritis.": Elsevier BV, April 2000.

Full Text

Vigna, SR. "Evolution of the cholecystokinin and gastrin peptides and receptors." American Zoologist 40, no. 2 (January 1, 2000): 287-295.

Full Text

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