Molecular Vision: Dratviman-Storobinsky, Mol Vis 2008; 14:2171-2179. Table 2

Table 2. Detection of cell loss in the retina and optic nerve in both models of injury, by fluorescence label versus nuclei staining (Hoechst) and TUNEL.

Models of injury				CRUSH n=40 % (±SD)		rAION n=40 % (±SD)
Retina	RGC loss	Thy1-CFP mice (n=20)	CFP 21 d (n=5)	77.4 (±7.4)		25.3 (±9.5)
		Thy1-CFP mice (n=20)	Hoechst 21d (n=5)	69.5 (±3.3)		22.9 (±14.7)
		TUNEL	apoptotic 1d/3d (n=5)	25%	40%	5%	20%
Optic nerve	OLG loss	CNPase-GFP mice (n=20)	CNPase 21d (n=5)	52.3 (±8.6)		27.4 (±4.6)
Optic nerve	OLG loss	CNPase-GFP mice (n=20)	Hoechst 21d (n=5)	51.1 (±5.3)		20.3 (±7.2)

Comparison of cell loss in the retina and optic nerve in both models of injury, by fluorescence (CFP or GFP) versus nuclei staining (Hoechst), at day 21. Our finding of greater RGC loss and axonal damage in the Thy1-CFP mice subjected to crush injury compared to the Thy1-CFP mice subjected to rAION induction indicated that the crush injury caused more damage than rAION. In both models, the damage progressed within days, and loss of oligodendrocytes could be detected on day 21, more in the crush model. We were also able to show that the optic nerve injury, induced in both crush and rAION models, led to anterograde RGC apoptosis. Apoptosis assays (TUNEL) at days 1 and 3 indicate apoptotic mechanism of the retinal ganglion cell loss, increasing towards day 3. Maximal RGC loss (irreversible loss) calculated for day 21 showed 77.4% in the crush model, and 25.3% for the rAION model.