Mark T. Nelson

University of Vermont


Election Year: 2019
Primary Section: 23, Physiology and Pharmacology
Secondary Section: 24, Cellular and Molecular Neuroscience
Membership Type: Member

Biosketch

Mark Nelson is known for his research on ion channels and calcium signaling in smooth muscle and endothelial cells, particularly for his work on electrical and local calcium signaling in the brain vasculature and urinary bladder. He was born in New York City, New York, and grew up in New Jersey. After graduating from Tufts University, Medford, Massachusetts with a degree in Mathematics and Biology, he went to Washington University, Saint Louis, Missouri, where he obtained a Ph.D. in Neural Science with Professor Mordecai Blaustein in 1980. He did postdoctoral work at the University of Maryland, Baltimore, and Universität Konstanz, Germany, sponsored by Professor Peter Läuger. Nelson joined the faculty of the University of Vermont in 1986 and became Chair of the Department of Pharmacology in 1995. He has a part-time Professorship at the University of Manchester and is a visiting Professor at the University of Oxford. Dr. Nelson is a member of the Vermont Academy of Arts and Sciences, Vermont Academy of Sciences and Engineering, and the National Academy of Sciences.

Research Interests

The Nelson laboratory's research interests include elucidating the mechanisms by which cerebral blood flow is controlled to meet the diverse and ever-changing demands of active neurons and how these mechanisms are disrupted in small vessel disease (SVD)-a major cause of stroke and dementia. Dr. Nelson and colleagues have unraveled many of the major mechanisms that control cerebrovascular function, including the discovery of local calcium signals ('sparks'), which counter-intuitively oppose vasoconstriction. They have recently shown that brain capillaries act as a neural activity-sensing network by initiating and transmitting an electrical signal, mediated by potassium channel activation, that propagates through the interconnected endothelial cells comprising the capillaries that line all blood vessels. This concept explains the rapid and coordinated delivery of blood to active neurons. Using a mouse model of a monogenic form of SVD, they have discovered early defects that result in a loss of this electrical signaling mechanism and impaired delivery of blood to active neurons-defects that involve changes in extracellular matrix composition. The near-term goals of Nelson laboratory researchers are to create an integrated view of electrical, calcium and related regulatory signaling mechanisms at molecular, biophysical, and computational-modeling levels by examining their operation in increasingly complex segments of the brain vasculature ex vivo, in vivo, and in silico. Ultimately, they propose to weave these research threads together to create a systems-level view of physiological signaling in the brain microcirculation, and test the concept that gradual degradation of this sensory web and the attendant progressive decay of cerebrovascular function contributes to SVDs of the brain.

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