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Mark T. Nelson, PhD, FAHA
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Mark T. Nelson, PhD, FAHA

Mark T. Nelson, PhD, FAHA

Education:

Doctoral Studies
Washington University, St. Louis, MO
Postdoctoral Training
University of Maryland, Baltimore, MD
Universität Konstanz, West Germany

Training:

Residency
Fellowship

Specialty:

Certifications:

Academic Appointments:

Chair, Department of Pharmacology

Professor, Department of Pharmacology

Professor, Department of Molecular Physiology & Biophysics

Biography:

Dr. Nelson is Chair and Professor of the Department of Pharmacology in the College of Medicine at the University of Vermont.  He received his B.A., with honors, in Mathematics and Biology from Tufts University in 1976 and his Ph.D. in Neural Sciences from Washington University in 1980.  His work has been supported mainly by NIH, NSF, and the American Heart Association.  He is a current member of the Vermont Academy of Sciences & Engineering (1999-) and an ad hoc member of the NIH Pharmacology Study Section (regular member 1998-2002).  He has served as Councilor of the Biophysical Society Council (1998-2002),  was awarded an Alexander von Humboldt-Stiftung Fellowship while at the Universität Konstanz (1981-82; 84), an American Heart Association Fellowship while at the University of Maryland (1980-81), and a National Science Foundation Summer Fellowship while at Swarthmore College (1974). He was a University Scholar at the University of Vermont (1996), an Established Investigator of the American Heart Association (1985-90), and an Honorable Mention Awardee from the American Heart Association for the Louis N. Katz Research Prize for Young Investigators (1982).  Dr. Nelson has lectured and published widely, served as a consultant to several corporations, and has a particular research interest in the properties and roles of ion channels in smooth-muscle function.  He and his wife, Inge, live in Jericho with their daughter.

Major Research Interests:

The overall goal of the research in Dr. Nelson's laboratory is to understand the control of smooth muscle cell function by the cell membrane. A combined approach, utilizing single cell isolation, single channel and macroscopic recording techniques, intracellular calcium and calcium spark measurements with conventional fluorescent imaging techniques, laser scanning, and confocal microscopy, diameter and membrane potential measurements in intact pressurized arteries, and expression of ion channels, is used to characterize the properties of calcium and potassium channels and ryanodine-sensitive calcium release channels. Calcium and potassium channels are the sites of action of several types of drugs that are used to treat cardiovascular disorders such as hypertension and angina. To understand the mechanisms of action of these and potentially novel agents, their effects on calcium and potassium channel behavior are being delineated.

Recent Grant Support

Grant Title: Coronary artery regulation by Ca2+ signaling and estrogen
Sponsor: National Institutes of Health
PI: Mark T. Nelson, Ph.D.

Grant Title: Special program in cellular and molecular neurobiology
Sponsor: National Institutes of Health
PI: Mark T. Nelson, Ph.D.

Grant Title: Ca2+ sparks and urinary bladder smooth muscle excitability
Sponsor: National Institutes of Health
PI: Mark T. Nelson, Ph.D.

Grant Title: Regulation of cerebral artery dilation
Sponsor: National Institutes of Health
PI: Mark T. Nelson, Ph.D.

Grant Title: Totman Center for human cerebrovascular research
Sponsor: R.W. & I. Totman Medical Research Fund
PI: Mark T. Nelson, Ph.D.

Grant Title: Mechanisms of cerebral resistance artery contraction
Sponsor: National Institutes of Health
Co-Investigator: Mark T. Nelson, Ph.D.; Joseph  E. Brayden, Ph.D. (PI)

Grant Title: Neural control of the gallbladder
Sponsor: National Institutes of Health
Co-Investigator: Mark T. Nelson, Ph.D.; Gary M. Mawe, Ph.D. (PI)

Grant Title: Potassium channel openers
Sponsor: GlaxoSmithKline, Corp.
PI: Mark T. Nelson, Ph.D.

Publications:

Representative Publications From a Total of 150

Nelson, M.T. and Blaustein, M.P.  (1981)  Effects of ATP and vanadate on calcium efflux from barnacle muscle fibers. Nature, 289:314-316.

Nelson, M.T., Standen, N.B., Brayden, J.E., and Worley, J.F.  (1988)  Noradrenaline contracts arteries by activating voltage-dependent calcium channels.  Nature, 336:382-385.

Standen, N.B., Quayle, J.M., Davies, N.W., Brayden, J.E., Huang, Y., and Nelson, M.T.  (1989) Hyperpolarizing vasodilators activate ATP-sensitive K+ channels in arterial smooth muscle. Science, 245:177-180.

Nelson, M.T., Cheng, H., Rubart, M., Santana, L.F., Bonev, A.D., Knot, H.J., and Lederer, W.J. (1995) Relaxation of arterial smooth muscle by calcium sparks.  Science, 270:633-637.

Jaggar, J.H., Porter, V.A., Lederer, W.J., and Nelson, M.T.  (2000)  Calcium sparks in smooth muscle. Am. J. Physiol., 278: C235-C256.  Cover page of journal.

Welsh, D.G., Morielli, A.D., Nelson, M.T., & Brayden, J.E.  (2002)  Transient receptor potential channels regulate myogenic tone of resistance arteries.  Circ. Res., 90:248-250.

Herrera, G.M. & Nelson, M.T.  (2002)  Differential regulation of SK and BK channels by Ca2+ signals from Ca2+ channels and ryanodine receptors in guinea-pig urinary bladder myocytes.  J. Physiol., 541:483-492.

Gomez, M.F., Bosc, L.V., Stevenson, A.S., Wilkerson, M.K., Hill-Eubanks, D.C., & Nelson, M.T.  (2003) Constitutively elevated nuclear export activity opposed Ca2+-dependent NFATc3 nuclear accumulation in vascular smooth muscle:  Role of JNK2 and Crm-1.  J. Biol. Chem., 278:46847-46853.

Amberg, G.C., Bonev, A.D., Rossow, C.F., Nelson, M.T., & Santana, L.F.  (2003) Modulation of the molecular composition of large conductance, CA(2+) activated K(+) channels in vascular smooth muscle during hypertension.  J. Clin. Invest., 112:717-724.

Earley, S. and Nelson, M.T.  (2006) Central role of Ca2+-dependent regulation of vascular tone in vivo.  J. Appl. Physiol. 101:10-11.

Jagodic, M.D., Pathirathna, S., Nelson, M.T., Mancuso, S., Joksovic, P.M., Rosenberg, E.R., Bayliss, D.A., Jevtovic-Todorovic, V., and Todorovic, S.M.  (2007)  Cell-specific alterations of T-type calcium current in painful diabetic neuropathy enhance excitability of sensory neurons.  J. Neurosci. 27:3305-3316.

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