Prior to my arrival in Rochester, I spent a brief time working as a postdoctoral fellow in the Department of Medicine, Manchester Royal Infirmary, UK, investigating the mechanisms of hypoxic vasodilation in small resistance arteries. This work has advanced our understanding of how calcium waves are generated and propagated in pancreatic and parotid acinar cells. The primary focus of my own research has been to elucidate the molecular mechanisms controlling the secretion of peptide hormones. Peptide hormones control many basic processes of life, including volume regulation, sugar metabolism, and neuronal excitability. I use a variation on the patch clamp method to monitor changes in cell membrane surface area, in combination with flash photolysis of caged compounds, fluorescence digital imaging, confocal microscopy, and molecular biology methods.
Mitochondria are critical components of cellular energy balance, calcium dynamics, and apoptosis.
Recently, these complex organelles have been revealed to be centrally involved in a wide variety of disease processes, notably in neurodegenerative disorders, diabetes and cardiomyopathy. Currently, I am using isolated neurohypophysial nerve endings to probe the physiological and pathophysiological basis for this regulation. My research focuses on understanding the mechanisms by which different agonists, which couple to the same signal transduction machinery, elicit different calcium signaling patterns and physiological end-points. In pancreatic acinar cells, stimulation by agonists which couple to the Gq class of G-protein coupled receptors results in the production of InsP 3 and release of stored ER calcium. Since a common second messenger appears to be responsible for producing the resultant calcium changes, differential modulation of the calcium signaling machinery may result in the production of these different calcium signaling patterns.