Associate Professor, Dept. of Pharmacology, University of Vermont, 7/06 to present

Associate Professor, Department of Surgery, section of Neurological Surgery, University of Vermont (secondary appointment), 7/06 to present.

Assistant Professor, Department of Surgery, section of Neurological Surgery, University of Vermont (secondary appointment), 7/00 to 6/06.

Assistant Professor, Dept. of Pharmacology, University of Vermont, 1/00 to 6/06.

Postdoctoral Fellow, Dept. of Pharmacology, University of Vermont, 10/97 to 12/99,
Supervisor: Prof. Mark T. Nelson

Research Associate, Dept. of Cell Physiology & Pharmacology, University of Leicester,
England, 10/95 to 10/97, Supervisor: Prof. N. B. Standen

Graduate Assistant, Dept. of Pharmacology, University of Vermont, 8/93 to 9/95, Thesis
Advisor: Prof. Joseph E. Brayden

The overall goal of my research is to understand how cerebral artery diameter is regulated during health and disease. A major emphasis in the lab is to understand the cellular mechanisms associated with pathological cerebral artery constriction following cerebral aneurysm rupture and subarachnoid hemorrhage (SAH). Aneurysmal SAH occurs in approximately 30,000 people each year in the United States and is associated with high rates of morbidity and mortality. Current treatment strategies for this type of stroke are limited, contributing to poor patient outcome.

Our research combines a variety of experimental techniques to study how blood released onto the brain surface causes changes in electrical activity and calcium signaling leading to smooth muscle contraction. Our studies have revealed that subarachnoid blood can have profound effects on plasma membrane Ca2+ and K+ channel activity, as well as the frequency of intracellular Ca2+ release events (Ca2+ sparks). We have also recently demonstrated fundamental changes in local and global calcium signaling within the neurovascular unit (neurons, astrocytes and parenchymal arterioles) of subarachnoid hemorrhage model animals. Specifically, in the context of brain slices where communication between neurons, astrocytes and the vasculature is intact (i.e., the intact neurovascular unit), we have novel and exciting evidence that subarachnoid hemorrhage causes a shift in neurovascular coupling from vasodilation to vasoconstriction.

Techniques in the lab include:
• patch clamp electrophysiology to measure ion channel activity
•laser scanning confocal microscopy, multi-photon microscopy and conventional epifluorescence microscopy to examine local and global intracellular calcium concentrations in arterial myocytes and astrocytic endfeet
•molecular biology and biochemical approaches including qualitative real- time PCR and western blot
•in vitro functional measurements of cerebral artery diameter.