Abstract
Purpose: :
To study the functionality of the mouse retinal ganglion cell (RGC) after optic nerve section (ONS) through electroretinographic recordings. The influence of photoreceptors lost in RGCs survival after ONS was further addressed by using mouse models of retinal degeneration.
Methods: :
Ganglion cell survival was analyzed histologically by comparing damaged (4, 7, 14, 21 and 30 days post-axotomy) and no damaged retinas. For RGC labelling, both optic nerves were exposed to dextran tetramethylrhodamine (DTMR). Hematoxilin labeling of mouse retinal sections allowed to analyze RGC survival after ONS, both in wild type or dystrophyc animals. Electroretinograms were carried out to assess retinal function of RGCs after ONS. Scotopic threshold response (STR) amplitude was measured and compared in both eyes (control and damaged) at 7, 14, and 21 days after section.
Results: :
No significant difference was observed in ganglion cell counts at four days post-axotomy compared to control eyes. A significant lost of RGCs was observed in the second week after injury. Wild type mice showed a cellular lost of 32.44% in the ganglion cell layer at two weeks after ONS and 37.40% at three weeks after lesion. However, in dystrophic mice, the cellular lost was 26.70% three weeks after axotomy. After ONS, a decrement in the STR amplitude was observed in lesioned eyes. However, response amplitude to greater stimuli were normal. One week after injury, the decrease of STR amplitude was no statistically significant, but recordings at two weeks post-ONS showed a significat decrease to 70%. This decrease in the STR amplitude was maintained for longer periods after ONS.
Conclusions: :
After ONS, the peak of maximum RGC death is in the second week after axotomy. Progressive decrease of RGC population after ONS induced a decrease in the amplitude of STR. The absence of photoreceptors seems to delay RGC death after axotomy.
Keywords: pathology: experimental • electroretinography: non-clinical • retinal degenerations: cell biology