About

Professor Erika D. Eggers leads the Eggers Laboratory of Retinal Neurophysiology at the University of Arizona. Her research focuses on the modulation of retinal synaptic signaling by lighting conditions and disease, with a particular emphasis on early diabetes. To explore these mechanisms, her lab employs a variety of techniques including single-cell electrophysiology, immunohistochemistry, fluorescent in-situ hybridization, and in vitro electroretinogram recordings (ERG). The lab is actively engaged in advancing understanding of how retinal function is affected by environmental and pathological factors, contributing to the broader field of visual neuroscience and disease pathology.

Research topics

• Neuroscience
• Chemistry
• Biology
• Medicine
• Endocrinology
• Biochemistry
• Internal medicine
• Ophthalmology

Selected publications

• Dopamine D1 Receptors Modulate glycinergic Inhibitory Inputs to OFF cone bipolar cells elicited by Optogenetic Activation of Amacrine Cells

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-12-02

  articleOpen accessSenior authorCorresponding

  Abstract Light evoked inhibition on OFF cone bipolar cells has been shown to be modulated by both background light levels and the Dopamine D1 Receptor. Since dopamine receptors are localized throughout the mouse retina, it is not known where in the light signaling cascade dopamine is modulating signals to OFF bipolar cells. The goal of this work was to develop a technique that allowed for the isolation of the amacrine to OFF bipolar cell circuit and determine if there are local changes in inhibition elicited by presynaptic amacrine cells onto OFF bipolar cells. To do this, we utilized the B6.Cg-Tg(Slc32al-COP4*H134R/EYFP) mouse line. These mice contain ChR2 in all the inhibitory cells in the retina. By optogenetically activating the amacrine cells, we were able to elicit inhibitory currents on bipolar cells independent of photoreceptor activation. Additionally, we were able to pharmacologically block inputs from photoreceptors while simultaneously isolating individual GABAergic and glycinergic inputs to OFF bipolar cells. While these optogenetically elicited currents were distinct from previously recorded light evoked currents, we found this as an effect way to measure changes in SKF38393 mediated reductions in glycinergic currents on OFF bipolar cells. However, we did not observe changes in GABAergic inhibition as we have previously seen in light evoked currents. Together, this gives a novel perspective on how dopamine differentially shapes inhibitory changes in the inner retina.

  PublisherDOI

• D1R- and D4R-Dependent Regulation of Retinal Light Adaptation in Diabetes

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-12-02

  articleOpen accessSenior author

  Abstract Diabetic retinopathy (DR) is considered a neurovascular disease, and key clinical features show impairments in visual acuity and electroretinogram (ERG) recordings. Dopamine, a critical regulator of light adaptation, is also reduced in diabetes and supplementation of dopamine or injection of dopamine agonists improve visual deficits in diabetic rodents and humans. We sought to examine how blocking D4Rs and D1Rs would affect ERG signaling in 6-week diabetic rodents. Blocking D4Rs with L745,870 significantly reduced dark-adapted A-wave amplitude in DM, but not non-DM retinas, with no change in a-wave implicit timing, suggesting diabetic alterations in D4R signaling in photoreceptors. Light-adapted (LA) recordings revealed blocking D4Rs significantly increased A-wave amplitude and delayed A-wave implicit timing in DM and non-DM retinas. B-wave amplitudes were elevated at the highest flash intensity, and rise time was significantly faster, indicating an inability to adjust to background light. D1R blockade with SCH-23390 had little effect on ERG recordings for both groups, aside from increased B-wave amplitude and delayed rise time in dark-adapted DM conditions towards the lower light intensities. While small, D4R blockade seems to have a bigger effect in DM conditions during light adaptation, suggesting that diabetes impairs the retina’s ability to adjust to light adaptation. These studies show that dopamine signaling in diabetes is perturbed and an important avenue for future investigation.

  PublisherDOI

• Early Diabetic Ca ²⁺ Handling Impairments in the Rod Bipolar Pathway

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-12-03

  articleOpen accessSenior authorCorresponding

  Abstract Background Previous work showed that electrically-evoked inhibition to Rod Bipolar Cells (RBC) is reduced in a mouse model of early diabetes. It is hypothesized that this is due to impaired Ca 2+ handling in the presynaptic amacrine cell, either through increased Ca 2+ buffering or decreased influx. To test this hypothesis and develop a mechanism for this effect, a model where direct optogenetic activation of inhibitory amacrine cells that expressed the light-activated channel ChR2 was used to isolate amacrine cell inputs to RBCs. Application of selective Ca 2+ channel blockers could then assess potential locations of amacrine Ca 2+ disruption. Using whole cell patch clamp electrophysiology, recordings were made from a 6 week diabetic population (DM) and vehicle injected non-DM animals. Results Robust GABA C receptor inhibitory currents were recorded from RBCs after ChR2 stimulus that were significantly diminished by the application of nifedipine to block L-type Ca 2+ channels in both DM and non-DM conditions. There were significant differences in the peak amplitude of these responses between DM and non-DM groups (p = 0.0146). However, in the non-DM group the decay tau of the response to the 50ms stimulus was significantly diminished by nifedipine ( τ p =0.0498, n = 5), but this was not seen in the DM group ( τ p = 0.9498, n=7). A 1s nifedipine-reduced response saw its decay tau increase in the DM group but not the non-DM. Ca 2+ - induced Ca 2+ release (CICR) blockade with ryanodine decreased responsivity equally between groups in the 1s stimulus but showed no significant kinetic changes. CICR blockade for a 50ms stimulus response showed significant kinetic changes in diabetes but otherwise reduced the response equally between DM and non-DM. Blockade of the mitochondrial Ca 2+ uniporter (MCU) had little effect on the optogenetic response. Conclusion This study presents evidence that diabetes alters amacrine cell output to the RBC unmasked through blockade of the L-type calcium channel, and the Endoplasmic Reticulum (ER). An apparent explanation for our results is that DM calcium buffering is dysregulated, leading to prolonged responses. The underlying mechanism for this alteration is complex and not yet clearly elucidated.

  PublisherDOI

• Impaired dopamine signaling in early diabetic retina: Insights from D1R and D4R agonist effects on whole retina responses

  Experimental Eye Research · 2024-08-14 · 3 citations

  articleOpen accessSenior authorCorresponding
  PublisherOA PDFDOI

• Visual Dysfunction in Diabetes

  Annual Review of Vision Science · 2023-05-10 · 16 citations

  reviewOpen access1st authorCorresponding

  Although diabetic retinopathy (DR) is clinically diagnosed as a vascular disease, many studies find retinal neuronal and visual dysfunction before the onset of vascular DR. This suggests that DR should be viewed as a neurovascular disease. Prior to the onset of DR, human patients have compromised electroretinograms that indicate a disruption of normal function, particularly in the inner retina. They also exhibit reduced contrast sensitivity. These early changes, especially those due to dysfunction in the inner retina, are also seen in rodent models of diabetes in the early stages of the disease. Rodent models of diabetes exhibit several neuronal mechanisms, such as reduced evoked GABA release, increased excitatory glutamate signaling, and reduced dopamine signaling, that suggest specific neuronal deficits. This suggests that understanding neuronal deficits may lead to early diabetes treatments to ameliorate neuronal dysfunction.

  PublisherOA PDFDOI

• Impaired Light Adaptation of ON-Sustained Ganglion Cells in Early Diabetes Is Attributable to Diminished Response to Dopamine D4 Receptor Activation

  Investigative Ophthalmology & Visual Science · 2022-01-25 · 8 citations

  articleOpen accessSenior author

  Purpose: Retinal neuronal signaling is disrupted early in diabetes, before the onset of the vascular pathologies associated with diabetic retinopathy. There is also growing evidence that retinal dopamine, a neuromodulator that mediates light adaptation, is reduced in early diabetes. Previously, we have shown that after 6 weeks of diabetes, light adaptation is impaired in ON-sustained (ON-s) ganglion cells in the mouse retina. The purpose of this study was to determine whether changes in the response to dopamine receptor activation contribute to this dysfunction. Methods: Single-cell retinal patch-clamp recordings from the mouse retina were used to determine how activating dopamine type D4 receptors (D4Rs) changes the light-evoked and spontaneous excitatory inputs to ON-s ganglion cells, in both control and 6-week diabetic (STZ-injected) animals. Fluorescence in situ hybridization was also used to assess whether D4R expression was affected by diabetes. Results: D4R activation decreased light-evoked and spontaneous inputs to ON-s ganglion cells in control and diabetic retinas. However, D4R activation caused a smaller reduction in light-evoked excitatory inputs to ON-s ganglion cells in diabetic retinas compared to controls. This impaired D4R signaling is not attributable to a decline in D4R expression, as there was no change in D4R mRNA density in the diabetic retinas. Conclusions: These results suggest that the cellular response to dopamine signaling is disrupted in early diabetes and may be amenable to chronic dopamine supplementation therapy.

  PublisherDOI

• Dopamine D1 and D4 receptors contribute to light adaptation in ON-sustained retinal ganglion cells

  Journal of Neurophysiology · 2021-11-24 · 14 citations

  articleOpen accessSenior authorCorresponding

  Dopamine by bright light conditions allows retinal neurons to reduce sensitivity to adapt to bright light conditions. It is not clear how and why dopamine receptors modulate retinal ganglion cell signaling. We found that both D1 and D4 dopamine receptors in photoreceptors and inner retinal neurons contribute significantly to the reduction in sensitivity of ganglion cells with light adaptation. However, light adaptation also requires dopamine-independent mechanisms that could reflect inherent sensitivity changes in photoreceptors.

  PublisherOA PDFDOI

• Inhibitory components of retinal bipolar cell receptive fields are differentially modulated by dopamine D1 receptors

  Visual Neuroscience · 2020 · 14 citations

  Senior authorCorresponding
  • Neuroscience
  • Chemistry
  • Biology

  During adaptation to an increase in environmental luminance, retinal signaling adjustments are mediated by the neuromodulator dopamine. Retinal dopamine is released with light and can affect center-surround receptive fields, the coupling state between neurons, and inhibitory pathways through inhibitory receptors and neurotransmitter release. While the inhibitory receptive field surround of bipolar cells becomes narrower and weaker during light adaptation, it is unknown how dopamine affects bipolar cell surrounds. If dopamine and light have similar effects, it would suggest that dopamine could be a mechanism for light-adapted changes. We tested the hypothesis that dopamine D1 receptor activation is sufficient to elicit the magnitude of light-adapted reductions in inhibitory bipolar cell surrounds. Surrounds were measured from OFF bipolar cells in dark-adapted mouse retinas while stimulating D1 receptors, which are located on bipolar, horizontal, and inhibitory amacrine cells. The D1 agonist SKF-38393 narrowed and weakened OFF bipolar cell inhibitory receptive fields but not to the same extent as with light adaptation. However, the receptive field surround reductions differed between the glycinergic and GABAergic components of the receptive field. GABAergic inhibitory strength was reduced only at the edges of the surround, while glycinergic inhibitory strength was reduced across the whole receptive field. These results expand the role of retinal dopamine to include modulation of bipolar cell receptive field surrounds. Additionally, our results suggest that D1 receptor pathways may be a mechanism for the light-adapted weakening of glycinergic surround inputs and the furthest wide-field GABAergic inputs to bipolar cells. However, remaining differences between light-adapted and D1 receptor-activated inhibition demonstrate that non-D1 receptor mechanisms are necessary to elicit the full effect of light adaptation on inhibitory surrounds.

  PublisherOA PDFDOI

• Early diabetes impairs ON sustained ganglion cell light responses and adaptation without cell death or dopamine insensitivity

  Experimental Eye Research · 2020 · 17 citations

  Senior authorCorresponding
  • Endocrinology
  • Internal medicine
  • Neuroscience
  PublisherOA PDFDOI

• The effects of early diabetes on inner retinal neurons

  Visual Neuroscience · 2020 · 46 citations

  1st authorCorresponding
  • Neuroscience
  • Chemistry
  • Ophthalmology

  Diabetic retinopathy is now well understood as a neurovascular disease. Significant deficits early in diabetes are found in the inner retina that consists of bipolar cells that receive inputs from rod and cone photoreceptors, ganglion cells that receive inputs from bipolar cells, and amacrine cells that modulate these connections. These functional deficits can be measured in vivo in diabetic humans and animal models using the electroretinogram (ERG) and behavioral visual testing. Early effects of diabetes on both the human and animal model ERGs are changes to the oscillatory potentials that suggest dysfunctional communication between amacrine cells and bipolar cells as well as ERG measures that suggest ganglion cell dysfunction. These are coupled with changes in contrast sensitivity that suggest inner retinal changes. Mechanistic in vitro neuronal studies have suggested that these inner retinal changes are due to decreased inhibition in the retina, potentially due to decreased gamma aminobutyric acid (GABA) release, increased glutamate release, and increased excitation of retinal ganglion cells. Inner retinal deficits in dopamine levels have also been observed that can be reversed to limit inner retinal damage. Inner retinal targets present a promising new avenue for therapies for early-stage diabetic eye disease.

  PublisherOA PDFDOI

Recent grants

• NIH Grant F32EY015629

  NIH · $91k · 2006

• Retinal Neuronal Signaling in Early Diabetes

  NIH · $2.9M · 2015–2026

• NIH Grant K99EY018131

  NIH · $86k · 2009

• NIH Grant R00EY018131

  NIH · $728k · 2013

• CAREER: The Role of Inhibition in light adaptation of the OFF Retinal Pathway

  NSF · $900k · 2016–2024

Frequent coauthors

• Peter D. Lukasiewicz

  Washington University in St. Louis

  16 shared

• Reece Mazade

  Emory University

  16 shared

• Johnnie M. Moore-Dotson

  University of Arizona

  12 shared

• Michael D. Flood

  University of Arizona

  11 shared

• Justin S. Klein

  Stanford University

  6 shared

• Botir T. Sagdullaev

  Regeneron (United States)

  5 shared

• Andrea Wellington

  University of Arizona

  5 shared

• Heddwen L. Brooks

  Tulane University

  5 shared

Education

• Postdoctoral Fellow, Ophthalmology and Visual Sciences

  Washington University

  2009

• PhD, Physiology and Biophysics

  University of Washington

  2003

• A.B., Physics

  Washington University

  1997

Awards & honors

• Selected for Leadership Development Program for Women ARVO,…