David Križaj is the John Frederick Carter Professor in Ophthalmology & Visual Sciences at the University of Utah School of Medicine, currently also serving as the Director of the Neuroscience Program at the University of Utah. He completed graduate training at the New York University School of Medicine and postdoctoral fellow in retinal neurobiology at University of California San Francisco. He joined faculty at UCSF before moving to Salt Lake City in 2007 to investigate synaptic transmission and ocular mechanotransduction. The goal of his research is to define the molecular rules that govern intraocular pressure, calcium regulation and visual signaling in the eye. Bioengineering approaches investigate cellular mechanisms that transduce pressure, strain, shear, swelling in retinal neurons and glia. Translational projects focus on developing treatments for glaucoma, diabetic retinopathy and corneal pain.
Research projects: Professor Križaj’s laboratory is interested in the relationship between intracellular signaling pathways and neurotransmission in the retina. The lab is interested in how non-conventional signaling pathways such as intracellular calcium stores, calcium transporters and store-operated calcium channels collaborate with voltage-operated signals to modulate graded exocytosis. For example, recent experiments elucidated the roles of ryanodine receptors, mitochondria and TRPC channels in spatiotemporal calcium signaling in photoreceptors, glial cells and retinal ganglion neurons. Other projects focus on how TRP channels integrate temperature, mechanical stress and lipid signals, and how translation of these sensory imputs impacts on parallel light-evoked inputs and survival in ganglion cells. A third project is focused on using in vivo multiphoton imaging to deifne the physiology of microglia within the retina.