The differential control of c-jun expression in regenerating sensory neurons and their associated glial cells.

Damage to the axons of adult sensory neurons results in massively increased expression of the protooncogene c-jun both in neurons and in the associated Schwann cells. The role of growth factors and axon contact in mediating this expression was investigated in dissociated cultures of adult sensory neurons and glial cells that expressed c-jun within 24 hr of plating. Trk, trkB, and trkC growth factor receptor genes were expressed in discrete subpopulations of sensory neurons but addition of NGF or brain-derived neurotrophic factor (BDNF) did not inhibit the expression of c-jun. Similarly, axon contact was not sufficient to decrease c-jun expression in glial cells. However, c-jun expression could be downregulated in glial cells, but not neurons, by treatment with cAMP or forskolin and increased by raising intracellular calcium levels. The results suggest that c-jun levels are differentially regulated in neurons and glial cells but that NGF or BDNF do not regulate c-jun expression in damaged neurons.