Differential and Prolonged Expression of Fos–lacZ and Jun–lacZ in Neurons, Glia, and Muscle Following Sciatic Nerve Damage

Abstract

Fos–lacZ and Jun–lacZ transgenic mice were used to assess the involvement of immediate-early genes in the axotomy–transcription coupling pathway triggered by sciatic nerve injury in neonates and adults. Nerve transection transiently induced Fos–lacZ in degenerating (neonatal) and regenerating (adult) motor, but not sensory, neurons. In contrast, Jun–lacZ was persistently up-regulated in both axotomized motor and sensory neurons in neonates and adults. Thus, expression of these genes did not predict neuronal death or survival. As Jun–lacZ was induced in some undamaged sensory neurons, this gene can be regulated by direct (axotomy) and indirect (transcellular) mechanisms. Indirect mechanisms also mediate expression of both genes in denervated muscle, Schwann cells in the distal and proximal stumps, and satellite cells in the DRG following axotomy. Thus, either these genes may regulate distinct sets of target genes in different cell types or they may subserve a single mechanism that is common to many cell types.