Figure 2. BIM is expressed in RGCs after axonal injury.

In young uninjured RGCs (Sham), BIM is not detected in RGCs. RGCs are marked genetically with CFP using B6.Thy1-CFP mice. In these mice 95% of RGCs express CFP and only a small percent of the other type of neurons in the ganglion cell layer, displaced amacrine cells, express the transgene²⁰,²¹. At the beginning of RGC death after CONC (3 days after injury) BIM colocalizes with the vast majority of CFP+ cells. BIM continues to be expressed in the RGC layer at 5 days and 7 days indicating it is expressed throughout the time when RGC death peaks. In glaucomatous DBA/2J mice, BIM is also expressed in RGCs (RGCs are also marked with the Thy1-CFP transgene; backcrossed into DBA/2J mice >20 times). BIM expression was not detected in all sections, but was present in RGCs in 4 out of 6 retinas examined. This expression is consistent with the asynchrony of DBA/2J glaucoma, with only some 10 month old animals undergoing active RGC loss²⁹. Also, in diseased retinas, BIM was not detected in every section likely reflecting the naturally-occurring sectorial pattern of RGC loss⁸. In addition, BIM expression was absent in 10 month old D2.Gpnmb mice (data not shown; D2.Gpnmb mice are a control strain of D2 mice that are wild-type for one of the genes that causes the iris disease and do not develop elevated IOP⁴⁰,⁴⁴). The lack of BIM expression in D2.Gpnmb RGCs indicates that change in BIM expression in DBA/2J RGCs is caused by the glaucomatous insult and not age or genetic background. These data show that BIM is expressed in axonally injured RGCs. Scale bar, 25 μm.