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
(520) 626-7137
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
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., & Lukasiewicz, P. D. (2006). GABAA, GABAC and glycine receptor-mediated inhibition differentially affects light-evoked signaling from mouse retinal rod bipolar cells. Journal of Physiology.
Herrmann, R., Heflin, S. J., Hammond, T., Lee, B., Wang, J., Gainetdinov, R. R., Caron, M. G., Eggers, E. D., Frishman, L. J., McCall, M. A., & Arshavsky, V. Y. (2011). Rod vision is controlled by dopamine-dependent sensitization of rod bipolar cells by GABA. Neuron, 72(1), 101-10.

Dark and light adaptation of retinal neurons allow our vision to operate over an enormous light intensity range. Here we report a mechanism that controls the light sensitivity and operational range of rod-driven bipolar cells that mediate dim-light vision. Our data indicate that the light responses of these cells are enhanced by sustained chloride currents via GABA(C) receptor channels. This sensitizing GABAergic input is controlled by dopamine D1 receptors, with horizontal cells serving as a plausible source of GABA release. Our findings expand the role of dopamine in vision from its well-established function of suppressing rod-driven signals in bright light to enhancing the same signals under dim illumination. They further reveal a role for GABA in sensitizing the circuitry for dim-light vision, thereby complementing GABA's traditional role in providing dynamic feedforward and feedback inhibition in the retina.

Eggers, E., Mazade, R. E., & Eggers, E. D. (2013). Light adaptation alters the source of inhibition to the mouse retinal OFF pathway. Journal of neurophysiology.

Sensory systems must avoid saturation to encode a wide range of stimulus intensities. One way the retina accomplishes this is by using both dim light-sensing rod and bright light-sensing cone photoreceptor circuits. OFF cone bipolar cells are a key point in this process, as they receive both excitatory input from cones and inhibitory input from AII amacrine cells via the rod pathway. However, in addition to AII amacrine cell input, other inhibitory inputs from cone pathways also modulate OFF cone bipolar cell light signals. It is unknown how these inhibitory inputs to OFF cone bipolar cells change when switching between rod and cone pathways or if all OFF cone bipolar cells receive rod pathway input. We found that one group of OFF cone bipolar cells (types 1,2, and 4) receive rod-mediated inhibitory inputs that likely come from the rod - AII amacrine cell pathway, while another group of OFF cone bipolar cells (type 3) do not. In both cases, dark-adapted rod dominant light responses showed a significant contribution of glycinergic inhibition, which decreased with light adaptation and was, surprisingly, compensated by an increase in GABAergic inhibition. As GABAergic input has distinct timing and spatial spread from glycinergic input, a shift from glycinergic to GABAergic inhibition could significantly alter OFF cone bipolar cell signaling to downstream OFF ganglion cells. Larger GABAergic input could reflect an adjustment of OFF bipolar cell spatial inhibition which may be one mechanism that contributes to retinal spatial sensitivity in the light.

Eggers, E. D., O'Brien, J. A., & Berger, A. J. (2000). Developmental changes in the modulation of synaptic glycine receptors by ethanol. Journal of Neurophysiology.