Dr. Keirstead received her Ph.D. in neurophysiology from Queen's University, Kingston, Canada, where she studied the role of neck muscle motoneurons and sensory afferents in the control of head movement in the laboratory of Dr. P. Ken Rose.
As a post-doctoral fellow in the laboratories of Dr. M. Rasminsky and Dr. A.J. Aguayo at McGill University, Dr. Keirstead examined the capabilities of retinal neurons to regenerate axons and form functional synaptic connections with central nervous system neurons.
Dr. Keirstead came to the University of Minnesota as a research associate in the Department of Physiology where she used calcium imaging techniques to study the regulation of intracellular calcium ion concentration in glial cells by neurotransmitters in the laboratory of Dr. Robert Miller. Dr. Keirstead continued these studies as an assistant professor in the Department of Ophthalmology.
Dr. Keirstead is an assistant professor in the Departments of Medicine and Physiology, and a member of the Stem Cell Institute.
Current interests include:
1) the functional characterization of stem cells at various stages of differentiation and their functional integration into host tissue after transplantation and
2) the regulation of intracellular calcium ion concentration and membrane conductances in retinal glial cells and neurons by neurotransmitters and neuromodulators.
My research involves the use of calcium imaging and electrophysiological techniques to examine the functional characteristics of stem cells in vitro as they differentiate into cells of various tissue types. This system provides a useful model for the development of functional characteristics of neurons and other cells in culture. Furthermore, our functional studies will permit us to better define the optimum degree of differentiation for the successful integration of transplanted stem cells into target tissues of host animals.
We also are interested in defining the functional changes that take place in retinal neurons and glial cells after optic nerve injury. Retinal glial cells (M|ller cells) have been shown to respond to optic nerve injury with changes in their gene expression within hours of the injury, and thus keenly "sense" the retinal microenvironment. This, and other reactions to optic nerve injury must be triggered by some interaction between the retinal ganglion cells whose axons are severed, and the M|ller cells which are distant from the injury.
We are examining the expression of purinergic and other neurotransmitter receptors on M|ller cells after optic nerve injury since others have shown that purinergic receptors are up-regulated after some retinal degenerative diseases.
We are also examining the ability of retinal ganglion cells to regulate intracellular calcium ion concentration within days of optic nerve injury to evaluate their functional status in the critical hours before they begin to die. An understanding of retinal ganglion and glial cell responses to injury will help us to better combat pathological processes in the retina.