Biesecker, Kyle2017-03-142017-03-142016-12https://hdl.handle.net/11299/185199University of Minnesota Ph.D. dissertation.December 2016. Major: Neuroscience. Advisor: Eric Newman. 1 computer file (PDF); iv, 88 pages.Blood flow is tightly regulated in the central nervous system to ensure neurons receive sufficient oxygen and glucose. When neuronal activity increases, nearby blood vessels dilate to increase local blood flow, a phenomenon termed functional hyperemia. Two key controversies have arisen concerning the mechanisms that underlie functional hyperemia. Firstly, the role of glial Ca2+ signaling in triggering vessel dilations is unclear. Some evidence suggests that glial Ca2+ signals precede vessel dilations, but blocking glial Ca2+ signaling does not alter functional hyperemia. Secondly, data has been presented arguing both for and against the ability of capillaries to actively dilate during functional hyperemia. Herein, I demonstrate that glial Ca2+ signaling does play a key role in regulating capillary diameter, but is not necessary for regulating arteriole diameter. Additionally, capillaries can actively dilate during functional hyperemia responses. These findings suggest that glial Ca2+ signaling contributes to blood flow regulation in the central nervous system by triggering capillary dilations during functional hyperemia.enCalciumCapillaryFunctional hyperemiaGliaNeurovascular couplingRetinaThesis or Dissertation