Abstract
Purpose: :
Glaucoma is a leading cause of blindness and currently research on the disease concentrates on the retinal ganglion cell (RGC) degeneration caused due to the models employed. It is also important to understand the long term effects of these models on other retinal cells such as the photoreceptors and also the processing of visual information in the brain in areas such as the visual cortex.
Methods: :
Ocular Hypertension (OHT) was induced in rats using the Morrison method in one eye. ERGs and VEPs were performed at 3, 8, 16 and 26 wks after OHT induction. Animals were dark adapted over night and anaesthetised with ketamine and dormitor. ERGs were recorded from the cornea using a platinum wire electrode and VEPs were recorded using a platinum needle electrode inserted under the skin over the visual cortex. Under dark adapted conditions flashes of white light were presented at a range of intensities from 10ucd to 10cd. Following 20 mins adaptation to a 20cd background illumination, a range of 0.1cd to 10cd flashes were presented.
Results: :
The amplitude (µV) of the dark adapted (scotopic) ERG a-wave was significantly reduced in the IOP elevated eye compared to the unoperated eye at 16 wks (-217 ± 54 and -411 ± 31, N=7, P<0.05. All results are from the highest light intensity used) and 26 wks (-150 ± 36 and -419 ± 33, N=8, P<0.01). The b-wave amplitude was also significantly reduced in the IOP elevated eye compared to the unoperated eye at 26 wks (520 ± 127 and 1270 ± 84, N=8, P<0.01). Under light adapted (photopic) conditions the b-wave was significantly reduced in the IOP elevated eye compared to the unoperated eye at 16 wks (152 ± 31 and 280 ± 15, N=6, P<0.05) and 26wks (128 ± 29 and 285 ± 22, N=7, P<0.01). Simultaneous recording of cortical VEPs showed that the VEP amplitudes (P1 to N1) did not differ between IOP elevated and unoperated sides under scotopic or photopic conditions.
Conclusions: :
The reductions in ERG a-wave and b-wave amplitudes following OHT induction suggest that this model of glaucoma not only causes RGC degeneration but also possible secondary degenerations of the rod and cone photoreceptors or at least a change in their functional abilities. However it was shown that cortical VEPs did not show detrimental effects after this procedure suggesting that there may be some compensation in the visual cortex for the RGC loss and possible photoreceptor damage caused by this model.
Keywords: electrophysiology: non-clinical • electroretinography: non-clinical • apoptosis/cell death