Fig. 5
From: Together JUN and DDIT3 (CHOP) control retinal ganglion cell death after axonal injury
Neither Jun, Ddit3, or combined Jun/Ddit3 deficiency alters axonal degeneration after mechanical optic nerve injury. To assess the role of JUN and DDIT3 in axonal degeneration, compound action potentials (CAPs) were recorded from WT, Jun, Ddit3, and combined Jun/Ddit3 animals 5 days after ONC, a time point when there is significant loss of CAP amplitudes in WT mice [43]. a Representative traces show that sham eyes from all genotypes had normal action potentials, while amplitudes were reduced about 80% in all cases after ONC. b Quantification of CAPs from WT, Jun, Ddit3, and combined Jun/Ddit3 animals showed that there were no differences among the CAP amplitudes of naïve, uninjured eyes of all genotypes (P > 0.05). All genotypes had significantly reduced amplitudes after ONC as compared to naïve animals (P < 0.001 for all comparisons). CAP amplitudes of Jun, Ddit3, and combined Jun/Ddit3 animals were not significantly different after ONC from those of control animals (P > 0.05, n = 4 for each genotype and condition)