Light exposure causes functional changes in the retina: increased photoreceptor cation channel permeability, photoreceptor apoptosis, and altered retinal metabolic function
Version of Record online: 10 JUL 2007
© 2007 The Authors. Journal Compilation © 2007 International Society for Neurochemistry
Journal of Neurochemistry
Volume 103, Issue 2, pages 714–724, October 2007
How to Cite
Yu, T.-Y., Acosta, M. L., Ready, S., Cheong, Y.-L. and Kalloniatis, M. (2007), Light exposure causes functional changes in the retina: increased photoreceptor cation channel permeability, photoreceptor apoptosis, and altered retinal metabolic function. Journal of Neurochemistry, 103: 714–724. doi: 10.1111/j.1471-4159.2007.04766.x
- Issue online: 10 JUL 2007
- Version of Record online: 10 JUL 2007
- Received March 31, 2007; revised manuscript received May 11, 2007; accepted June 6, 2007.
- ion gating;
- lactate dehydrogenase;
- P23H rat;
- retinal degeneration
Light exposure induces retinal photoreceptor degeneration and retinal remodeling in both the normal rat retina and in animal models of retinal degeneration. Although cation entry is one of the triggers leading to apoptosis, it is unclear if this event occurs in isolation, or whether a number of pathways lead to photoreceptor apoptosis following light exposure. Following light exposure, we investigated the characteristics of cation entry, apoptotic markers [using terminal deoxynucleotidyl transferase (EC 126.96.36.199) dUTP nick-end labeling (TUNEL) labeling] and metabolic properties of retina from Sprague–Dawley (SD) rats and a rat model of retinitis pigmentosa [proline-23-histidine (P23H) rat]. Assessment of cation channel permeability using agmatine (AGB) labeling showed that excessive cation gating accompanied the series of anomalies that occur prior to photoreceptor loss. Increased AGB labeling in photoreceptors was seen in parallel with the appearance of apoptotic photoreceptors detected by TUNEL labeling with only a smaller proportion of cells colocalizing both markers. However, SD and P23H retinal photoreceptors differed in the amounts and colocalization of AGB gating and TUNEL labeling as a function of light exposure. Finally, reduced retinal lactate dehydrogenase levels were found in SD and P23H rat retinas after a 24-h light exposure period. Short-term (2 h) exposure of the P23H rat retina caused an increase in lactate dehydrogenase activity suggesting increased metabolic demand. These results suggest that energy availability may be exacerbated during the early stages of light exposure in susceptible retinas. Also, the concomitant observation of increased ion gating and TUNEL labeling suggest the existence of at least two possible mechanisms in light-damaged retinas in both SD and the P23H rat retina.