Selective degeneration of rod photore-JunB, and JunD) was observed in photoreceptors, Mu ¨ller ceptor cells in the retinal degenerative (rd) mouse prior cell nuclei were transiently immunoreactive for c-Jun on to their complete maturation is thought to result from P11. The incidence of c-Fos-positive photoreceptors elevated cyclic guanosine monophosphate (cGMP) levels peaked sharply at P12, 1 day earlier than the peak in owing to the inherited defect in cGMP-phosphodiesterase. apoptosis. Furthermore, the population of c-Fos-positive To investigate potential signaling pathways which might photoreceptors was distinct from apoptotic photoreceplead to apoptotic death of photoreceptors in the rd retina, tors exhibiting chromatin condensation. The aberrant exthe expression of immediate-early genes (IEG) of the pression of c-Fos protein in rod photoreceptors immediactivating protein-1 transcription factor (AP-1) family ately prior to their death in the rd mouse raises the possiwas examined. Increasing numbers of apoptotic photorebility that c-Fos may be directly or indirectly involved in ceptor nuclei were observed in the outer nuclear layer of triggering the apoptotic cascade. Furthermore, the addithe rd mouse beginning at postnatal day (P) 10. The peak tional finding of c-Jun induction in Mu ¨ller glia suggests incidence of apoptotic cells was observed at P13; by P16, that the IEG response to photoreceptor degeneration inalmost the entire population of photoreceptors had been volves both intra-and intercellular signal transduction lost. Although c-Fos-like immunoreactivity was absent pathways.