EXPRESSION OF C-JUN PROTEIN IN DEGENERATING RETINAL GANGLION-CELLS AFTER OPTIC-NERVE LESION IN THE RAT

Axonal lesions to the optic nerve (ON) induce c-Jun expression in reti nal ganglion cells (RGCs) of the rat in vivo. Detailed investigations using retrograde tracers, and double labeling studies for c-Jun and re generation-associated factors, such as the growth-associated protein G AP-43, have suggested that this upregulation of c-Jun is part of a cel l body response in an abortive attempt of affected RGCs to survive and regenerate an axon. On the other hand, prolonged expression of c-Jun protein has in several paradigms of neurodegeneration been linked to t he induction of apoptotic cell death. In the present study, we examine d the time course and subcellular localization of c-Jun protein by imm unocytochemistry on retinal sections after optic nerve crush and carri ed out double labeling for c-Jun protein and DNA strand breaks to dete ct apoptosis on the same sections. Several days after ON lesion, a sub population of RGCs was detected in which c-Jun protein was not confine d to the nucleus, but also located in the cytoplasm. In addition, RGCs were seen that displayed morphological signs of apoptosis, DNA strand breaks, and c-Jun immunoreactivity at the same time. Therefore, c-Jun expression is not confined to intact or regenerating ganglion cells, but also occurs in cells that are destined to die. Our results suggest that the decision to undergo either fate depends on additional signal ing events that modulate the transcriptional actions of c-Jun. (C) 199 7 Academic Press.