• Minnesota State University, Moorhead, BA, Biology and Chemistry, 2004

• Eric Newman , Ph.D.

Research Description:

One of the fundamental aspects of healthy brain function is the spatial and temporal control of blood flow to meet increased energy demands in regions of neuronal activity. The fundamental cellular mechanisms underlying this response, termed functional hyperemia, are not well understood. Recent evidence suggests that glial cells are the primary mediators of neurovascular coupling in the brain. A previous student in Dr. Newman's lab, Monica Metea, demonstrated in the rat retina that light and glial stimulation evoke both vasodilations and vasoconstrictions. The generation of bi-directional vasomotor activity raises the question of how such responses are controlled. Monica demonstrated that nitric oxide is an important modulator of this response. Low levels of nitric oxide in the retina result in a primarily vasodilatory response while high levels result in increased vasoconstriction. I am now investigating whether oxygen, another important small molecule with an important function in many biochemical pathways, can also modulate neurovascular coupling. In whole mount retinas exposed to 20% oxygen, light stimulation results in vasodilation mediated by the combined action of EETs and prostaglandins. Retinas exposed to 100% oxygen, in contrast, show both light-evoked vasodilation and vasoconstriction. In high oxygen, vasodilations are mediated entirely by EETs, while vasoconstrictions are mediated by 20-HETE. The increase in 20-HETE synthesis and absence of prostaglandin-mediated vasodilation in oxygen appear to be responsible for the differences in light-evoked vasomotor responses in the two different concentrations of oxygen.

Another project that I am working on is related to the disruption of functional hyperemia in diabetic retinopathy. It has been shown that light stimulated vascular responses are diminished in diabetic patients. I have found the same to be true in a Streptozotocin model of diabetes in rats. Based on preliminary experiments, it appears that inhibiting production of NO by the inducible form of nitric oxide synthase (iNOS) may be enough to restore normal neurovascular responses to diabetic retinas.

Committee Members:

• Eric A. Newman

• Paulo Kofuji (chair)

• Esam E. El-Fakahany

• Cheryl Olman

Lab Rotations:

• PUBH 6450 Biostatistics I
• PUBH 6451 - Biostatistics II
• PHYS 5201 Computational Neuroscience I
• CMB 8361 Neuro-Immune Interactions

Graduate Level Minor:

• Statistical and Computational Analysis

Conferences Attended and Presentations:

• Gordon Research Conference: Glial Biology - March, 2009
• Glia in Health and Disease - July, 2008
• Cerebral Blood flow and Metabolism - April, 2008
• US Japan Meeting for Glial Research - March, 2008
• Society for Neuroscience - Fall 2005, 2006, 2007
• Americal Society for Biochemistry and Molecular Biology - June, 2004
• Minnesota Academy of Sciences - 2003, 2004
• Midwest Regional Developmental Biology Meeting and
• Singer Symposium - 2004

• MinnCResT Fellowship (2009-2010)
• 3M fellowship (2005-2009)
• Stark Award (2008)

• Society for Neuroscience

• Kathmandu, Nepal