INJURY-ASSOCIATED INDUCTION OF GAP-43 EXPRESSION DISPLAYS AXON BRANCHSPECIFICITY IN RAT DORSAL-ROOT GANGLION NEURONS

Peripheral nerve injury results in the increased synthesis and axonal transport of the growth-associated protein GAP-43 in dorsal root gangl ion (DRG) neurons, coincident with regenerative growth of the injured peripheral axon branches. To determine whether the injury-associated s ignalling mechanism which leads to GAP-43 induction also operates thro ugh the central branches of DRG axons, we used immunocytochemistry to compare the expression of GAP-43 in adult rat DRG neurons 2 weeks afte r dorsal root crush lesions (central axotomy) or peripheral nerve crus h lesions (peripheral axotomy). In uninjured ganglia, a subpopulation of smaller DRG neurons expresses moderate levels of GAP-43, whereas la rger neurons generally do not. At 2 weeks following peripheral axotomy , virtually all axotomized neurons, large and small, express high leve ls of GAP-43. At 2 weeks following dorsal root lesions, no increase in GAP-43 expression is detected. Thus, the injury-associated up-regulat ion of GAP-43 expression in DRG neurons is triggered by a mechanism th at is responsive to injury of only the peripheral, and not the central , axon branches. These findings support the hypothesis that GAP-43 ind uction in DRG neurons is caused by disconnection from peripheral targe t tissue, not by axon injury per se.