All ETDs from UAB

Advisory Committee Chair

Timothy W Kraft

Advisory Committee Members

Lynn E Dobrunz

John J Hablitz

Robin A J Lester

Steven J Pittler

Document Type


Date of Award


Degree Name by School

Doctor of Philosophy (PhD) Heersink School of Medicine


Constant light exposure has long been known to induce photoreceptor degeneration. However, it is not known whether photoreceptors alter their physiology to adapt to the environmental stress caused by constant light exposure. In this study, we have developed a slow light damage model in rats to study changes in single rod physiology and retinal morphology after light damage. Rod physiology was documented by single rod recording using a suction electrode at 3 days (R3), 5 days (R5), 15 days (R15), and 30 days (R30) after 10 days of light damage, or sham light damage for controls. In addition, we used electroretinogram (ERG) and quantitative histology to monitor changes in retinal physiology and morphology at each time point. Light damage resulted in a 26% loss in area of the Outer Nuclear Layer (ONL) on the vertical meridian at R30. This loss was specific to the ONL, as the Inner Nuclear Layer (INL) area did not demonstrate changes in area. The Outer Segment (OS) length was significantly shorter at R3 and R5, but by R15 OS length recovered similar to age-matched controls. Physiologically, we found that after light damage, surviving rods have lower sensitivity to light. Specifically, the I1/2 (flash strength that elicits half-maximal response amplitude) was increased by two-fold at R3 when compared to age-matched controls. However, Rmax (maximal response), single photon response amplitude, and phototransduction gain were not affected by light damage. Changes in light sensitivity were transient, since after R3, sensitivity to light recovered to a level that is not different from the age-matched control group. Furthermore, a iv transient acceleration in recovery of the light response was observed at R3 and R5 when compared to age-matched controls. The dominant time constant (τ) was decreased by almost half at R3, and a third at R5, but recovered to the value of the control group by R15. Our results demonstrate that transient light damage causes prolonged but reversible physiological changes in the surviving rods and suggest that mechanisms controlling the phototransduction cascade could be involved in this process.