Ageing and the effect of repeated intraocular pressures on retinal function

© 2010 Jason CharngAim:To investigate the effects of ageing on retinal functions as well as that of repeated insults have on the older retina. Material and methods:Electroretinograms were collected and decomposed into retinal layer-specific responses and compared between two age groups of Sprague-Dawley rats (3 month old, n=16; 18 month old, n=16). These responses were further analysed with a modified correlation to consider the presence of specific downstream losses in the data. The same groups were then exposed to repeated insults (anterior chamber cannulation) with acute IOP challenge in one eye (60 mmHg) or a normal IOP in the contralateral cannulated eye (15 mmHg). The IOP insults were sustained for 60 minutes and were repeated four times with 7 days recovery between successive bouts. At the end of this four week period the eyes were harvested to quantify for Thy1 mRNA via polymerase chain reaction, a marker of ganglion cell stress. Results:Ageing produces an improved photoreceptor sensitivity in the presence of reduced photoreceptor amplitudes. A reduced amplitude is also found in the ON-bipolar cell b-wave but not the ganglion cell derived scotopic threshold response. Further analysis found evidence for a specific photoreceptor amplitude loss with age but that the increase in sensitivity lead to normal retinal ganglion cell outputs. In the young cannulated eyes, we find stress from surgery and IOP acts to upregulate photoreceptor and ON-bipolar cell sensitivities, producing normal ganglion cell function. However, in the old animals, the cannulation-related stress was adequate to cause non-selective dysfunction of retinal cells. As expected, Thy1 indicated similar levels of stress in eyes exposed to 60 mmHg in both ages, however showed no age effect. Conclusion:The experiments find evidence for plasticity in retinal function in response to ageing and stress, which acts to maintain normal retinal ganglion cell outputs. This adaptive capacity following stress is lost in older eyes, producing a downstream ganglion cell dysfunction. Further investigations are needed to ascertain the exact mechanisms underlying such alterations, which can possibly lead to novel therapeutic advances