Erika Eggers, PhD: All Eyes on Research

Friday, August 23, 2019

When we step out of a dark room into the daylight, our vision initially is overwhelmed and we are blinded by the sudden bright light. Our eyes quickly adjust back to normal through a process called light adaptation – a change in the sensitivity of neurons in the retina of the eye, a crucial function of our visual system. The mechanisms that give our eyes the ability to adapt to dim or bright light conditions are not well understood.

Erika Eggers, PhD, associate professor of physiology and biomedical engineering, and member of the BIO5 Institute, is studying the changes that occur in retinal cells during the process of light adaptation in the retina. Previous work has suggested that release of the chemical dopamine from retinal neurons is responsible for light adaptation. Dopamine is the chemical neurotransmitter we generally associate with pleasure sensation in the brain.

It turns out that certain retinal neurons normally release tiny amounts of dopamine. Photons of light generate minute electrical signals in the retina and dopamine seems to control the neuron-to-neuron relay of these electrical signals to the optic nerve and then to the brain. Light adaptation involves changes in the release of dopamine which, in turn, alters the sensitivity of electrical signaling to the brain’s visual cortex. 

Dr. Eggers and her research team in the Eggers Laboratory of Retinal Neurophysiologywill determine what changes are occurring in the retina to allow adaptation to increasing light levels and determine how dopamine is changing visual signaling. 

What makes this research even more important is Dr. Eggers’ finding that changes of light adaptation seem to be associated with early stages of diabetes. “During adaptation from dim to bright environments, changes in retinal signaling are mediated, in part, by dopamine. Dopamine dysfunction is linked with vision impairments in diabetic retinopathy, a leading cause of blindness in adults. Determining how dopamine is changing visual signaling could have an impact on developing treatments for this and other visual diseases,” explained Dr. Eggers.

Dr. Eggers and her team’s most recent article published in the Journal of Neurophysiology, “Dopamine D1 Receptor Activation Reduces Local Inner Retinal Inhibition to Light-Adapted Levels.”found further evidence linking dopamine and retina light processing. This could provide a foundation for future studies to determine therapies that may combat vision loss associated with diabetic retinal damage.  

In 2016, Dr. Eggers received a five-year, $900,000 National Science Foundation CAREER Award to explore the mechanisms of dopamine signaling as one of the neurotransmitter chemicals partly responsible for light adaptation in the retina. NSF CAREER Awards are the agency's most prestigious honor for junior faculty members. She also is principal investigator of a $1.9 million project funded by the National Eye Institute of the National Institutes of Health, “Retinal Neuronal Signaling in Early Diabetes,”with additional support from the International Retinal Research Foundation, using electrophysiological and anatomical techniques to study the diabetes-associated retinal changes.

The Arizona RETINA Project

Dr. Eggers’s NSF CAREER Award also supports a community outreach program she developed, the Arizona RETINA Project(Researchers Educating Tucson in Natural-Light Adaptation). Now in its fourth year, the program sponsors UA undergraduate students to educate the community on how light adaptation works and the importance of this process for normal vision. By participating in community events, such as the annual Tucson Festival of Books, and publishing a blog on vision research, the program aims to increase interest in science for high school students and the public.

“Retinal Neuronal Signaling in Early Diabetes” is supported by the National Eye Institute of the National Institutes of Health under grant No. EY02602701. “The Role of Inhibition in Light Adaptation of the OFF Retinal Pathway” is supported by the National Science Foundation under grant No. 1552184.