Injury‐associated induction of GAP‐43 expression displays axon branch specificity in rat dorsal root ganglion neurons

Abstract

Peripheral nerve injury results in the increased synthesis and axonal trasnport of the growth‐associated protein GAP‐43 in dorsal root ganglion (DRG) neurons, coincident with regenerative growth of the injured peripheral axon branches. To determine wheter the injury‐associated signalling mechanism which leads to GAP‐43 induction also operates through the central branches of DRG axons, we used immunocytochemistry to compare the expression of GAP‐43 in adult rat DRG neurons 2 weeks after dorsal root crush lesions (central axotomy) or peripheral nerve crush lesions (peripheral axotomy). In uninjured ganglia, a subpopulation of smaller DRG neurons expresses moderate levels of GAP‐43, whereas larger neurons generally do not. At 2 weeks following peripheral axotomy, virtually all axotomized neurons, large and small, express high levels of GAP‐43. At 2 weeks following dorsal root lesions, no increase in GAP‐43 expression is detected. Thus, the injury‐associated up‐regulation of GAP‐43 expression in DRG neurons is triggered by a mechanism that is responsive to injury of only the peripheral, and not the central, axon branches. These findings support the hypothesis that GAP‐43 induction in DRG neurons is caused by disconnection from peripheral target tissue, not by axon injury per se. © 1993 John Wiley & Sons, Inc.