Erika D Eggers

Erika D Eggers

Associate Professor, BIO5 Institute
Associate Professor, Biomedical Engineering
Associate Professor, Neuroscience - GIDP
Associate Professor, Physiological Sciences - GIDP
Associate Professor, Physiology
Primary Department
Department Affiliations
Contact
(520) 626-7137

Work Summary

Work Summary

My laboratory studies how the retina takes visual information about the world and transmits it to the brain. We are trying to understand how this signaling responds to changing amounts of background light and becomes dysfunctional in diabetes.

Research Interest

Research Interest

The broad goal of research in our laboratory is to understand how inhibitory inputs influence neuronal signaling and sensory signal processing in the healthy and diabetic retina. Neurons in the brain receive inputs that are both excitatory, increasing neural activity, and inhibitory, decreasing neural activity. Inhibitory and excitatory inputs to neurons must be properly balanced and timed for correct neural signaling to occur. To study sensory inhibition we use the retina, a unique preparation which can be removed intact and can be activated physiologically, with light, in vitro. Thus using the retina as a model system, we can study how inhibitory synaptic physiology influences inhibition in visual processing. This intact system also allows us to determine the mechanisms of retinal damage in early diabetes. Keywords: neuroscience, diabetes, vision, electrophysiology, light

Publications

Moore-Dotson, J. M., Beckman, J. J., Mazade, R. E., Hoon, M., Bernstein, A. S., Romero-Aleshire, M. J., Brooks, H. L., & Eggers, E. D. (2016). Early Retinal Neuronal Dysfunction in Diabetic Mice: Reduced Light-Evoked Inhibition Increases Rod Pathway Signaling. Investigative ophthalmology & visual science, 57(3), 1418-30.
BIO5 Collaborators
Heddwen L Brooks, Erika D Eggers

Recent studies suggest that the neural retinal response to light is compromised in diabetes. Electroretinogram studies suggest that the dim light retinal rod pathway is especially susceptible to diabetic damage. The purpose of this study was to determine whether diabetes alters rod pathway signaling.

Eggers, E. D., Mazade, R. E., & Klein, J. S. (2013). Inhibition to retinal rod bipolar cells is regulated by light levels. Journal of neurophysiology, 110(1), 153-61.

The retina responds to a wide range of light stimuli by adaptation of retinal signaling to background light intensity and the use of two different photoreceptors: rods that sense dim light and cones that sense bright light. Rods signal to rod bipolar cells that receive significant inhibition from amacrine cells in the dark, especially from a rod bipolar cell-activated GABAergic amacrine cell. This inhibition modulates the output of rod bipolar cells onto downstream neurons. However, it was not clear how the inhibition of rod bipolar cells changes when rod signaling is limited by an adapting background light and cone signaling becomes dominant. We found that both light-evoked and spontaneous rod bipolar cell inhibition significantly decrease with light adaptation. This suggests a global decrease in the activity of amacrine cells that provide input to rod bipolar cells with light adaptation. However, inhibition to rod bipolar cells is also limited by GABAergic connections between amacrine cells, which decrease GABAergic input to rod bipolar cells. When we removed this serial inhibition, the light-evoked inhibition to rod bipolar cells remained after light adaptation. These results suggest that decreased inhibition to rod bipolar cells after light adaptation is due to decreased rod pathway activity as well as an active increase in inhibition between amacrine cells. Together these serve to limit rod bipolar cell inhibition after light adaptation, when the rod pathway is inactive and modulation of the signal is not required. This suggests an efficiency mechanism in the retina to limit unnecessary signaling.

Mazade, R. E., & Eggers, E. D. (2016). Light adaptation alters inner retinal inhibition to shape OFF retinal pathway signaling. Journal of Neurophysiology.
Flood, M. D., Moore-Dotson, J. M., & Eggers, E. D. (2016). D1 receptors modulate retinal rod bipolar cell inhibition. TBD.
Sagdullaev, B. T., Eggers, E. D., Purgert, R., & Lukasiewicz, P. D. (2011). Nonlinear interactions between excitatory and inhibitory retinal synapses control visual output. The Journal of neuroscience : the official journal of the Society for Neuroscience, 31(42), 15102-12.

The visual system is highly sensitive to dynamic features in the visual scene. However, it is not known how or where this enhanced sensitivity first occurs. We investigated this phenomenon by studying interactions between excitatory and inhibitory synapses in the second synaptic layer of the mouse retina. We found that these interactions showed activity-dependent changes that enhanced signaling of dynamic stimuli. Excitatory signaling from cone bipolar cells to ganglion cells exhibited strong synaptic depression, attributable to reduced glutamate release from bipolar cells. This depression was relieved by amacrine cell inhibitory feedback that activated presynaptic GABA(C) receptors. We found that the balance between excitation and feedback inhibition depended on stimulus frequency; at short interstimulus intervals, excitation was enhanced, attributable to reduced inhibitory feedback. This dynamic interplay may enrich visual processing by enhancing retinal responses to closely spaced temporal events, representing rapid changes in the visual environment.