The broad goal of research in my laboratory is to understand how light information is sensed and processed in the retina and how this processing changes during retinal disease. The retina is the neural layer at the back of the eye that senses light information. Neurons in the retina receive inputs that are both excitatory, increasing neural activity, and inhibitory, decreasing neural activity. Inhibitory signaling in the retina is thought to be important for much of the processing done there, but the details of the interaction between excitatory and inhibitory signaling is not well understood.
The retina is a unique preparation which can be removed intact and can be activated physiologically, with light, in vitro. We can then make electrical recordings of the signaling from retinal neurons during their natural behavior. By studying inhibitory electrical signaling in the retina I can understand how light information is processed into the visual signal that our brain senses. Additionally, we can use information about how the healthy retina works to determine how disease states, such as glaucoma and diabetic retinopathy, cause retinal dysfunction. Ultimately, understanding which neurons fail to function properly and why can help to restore sight.
Ph. D., Physiology and Biophysics, University of Washington, 2003
B.A., Physics, Washington University, 1997
Research & Interests
Diabetic neuronal damage
Mazade EM* and Eggers ED. Light adaptation alters the source of
inhibition to the mouse retinal OFF pathway. Journal of Neurophysiology,
(2013) 110(9): 2113-2128.
Eggers ED, Klein JS* and Moore-Dotson JM*. Slow changes in Ca2+ cause
prolonged release from GABAergic amacrine cells. Journal of Neurophysiology.
(2013) 110(3): 709-719.
Eggers ED, *Mazade EM and *Klein JS. Rod Bipolar cells have distinct rod
and cone pathways of inhibition. Journal of Neurophysiology. (2013)
Herrmann R, Heflin SJ, Hammond T, Lee B, Wang J, Gainetdinov RR,
Caron MG, Eggers ED, Frishman LJ, McCall MN and Arshavsky VY.
Rod vision is controlled by dopamine-dependent sensitization of
rod bipolar cells by GABA. Neuron. (2011) 72(1): 101-110.
Sagdullaev BT, Eggers ED, Purget R and Lukasiewicz PD.
Nonlinear Interactions between Excitatory and Inhibitory Retinal
Synapses Control Visual Output. Journal of Neuroscience.
(2011) 31(42): 15102-15112.
Eggers ED and Lukasiewicz PD. Multiple pathways of inhibition
shape bipolar cell responses in the retina. Visual Neuroscience.
(2011) 28(1): 95-108.
Eggers ED and Lukasiewicz PD. Interneuron circuits tune inhibition
in retinal bipolar cells. Journal of Neurophysiology. (2010) 103: 25-37.
Schubert T, Kerschensteiner D, Eggers ED, Misgeld T, Kerschensteiner M,
Lichtman J, Lukasiewicz PD and Wong ROL. Development of presynaptic
inhibition onto retinal bipolar cell axonal terminals is subclass-specific.
Journal of Neurophysiology. (2008) 100: 304-16.
Eggers ED, McCall MA and Lukasiewicz PD. Presynaptic inhibition
differentially shapes transmission in distinct circuits in the mouse retina.
Journal of Physiology. (2007) 582: 569-582.
Eggers ED and Lukasiewicz PD. Receptor and transmitter release properties
set the time course of retinal inhibition. Journal of Neuroscience.
(2006) 26: 9413-9425.
Eggers ED and Lukasiewicz PD. GABAA, GABAC and glycine receptor-mediated
inhibition differentially affects light-evoked signaling from mouse retinal rod
bipolar cells. Journal of Physiology. (2006) 572: 215-225.
Eggers ED and Berger AJ. Mechanisms for the Modulation of Native Glycine
Receptor Channels by Ethanol. Journal of Neurophysiology. (2004)
Sebe JY, Eggers ED, and Berger AJ. Differential effects of ethanol on
GABAA and glycine receptor-mediated synaptic currents in brain stem
motoneurons. Journal of Neurophysiology. (2003) 90: 870-875.
Eggers ED, O'Brien JA, and Berger AJ. Developmental changes in the
modulation of synaptic glycine receptors by ethanol. Journal of
Neurophysiology (2000) 84: 2409-2416.
Awards & Honors
NIH Pathways to Independence Award, 2008
University of Arizona College of Engineering
Department of Biomedical Engineering 1127 E James E. Rogers Way P.O. Box 210020 Tucson, AZ 85721-0020