Primary sensory neurons are capable of successful regenerative growth
in response to peripheral nerve but not dorsal root injury. The presen
t study is concerned with the differential expression of the mRNA for
GAP-43, a growth-associated protein, in these sensory neurons, in resp
onse to injury of their central or peripheral axonal branches. Periphe
ral axotomy resulted in an elevation in message detectable within 24 h
r, using Northern blot and in situ hybridization, which was maintained
for 30 d, whereas dorsal root section produced no change except a tra
nsient and small increase if the axotomy was immediately adjacent to t
he dorsal root ganglia (DRG). Dorsal root section had no effect on GAP
-43 mRNA levels in the dorsal horn or in neighboring intact DRG. It al
so failed to alter the laminar boundaries of the GAP-43 central termin
al labeling produced by peripheral nerve section, even though vacant s
ynaptic sites were produced in unstained laminae by this procedure. Th
is indicates that the location of GAP-43 immunolabeling in the central
terminals of primed sensory cells may not depend only on the location
of vacant synaptic sites. We conclude that distinct control mechanism
s regulate the response of DRG neurons to peripheral nerve and dorsal
root injury, and these may be related both to the glial environment an
d the particular target influences exerted on the central and peripher
al branches of the primary sensory neuron. Central denervation alone i
s insufficient to upregulate GAP-43 levels, and this may explain the r
elative absence of collateral sprouting after the production of centra
l vacant synaptic sites. The failure of dorsal root section to increas
e GAP-43 expression may contribute to the poor regenerative response i
nitiated by such lesions.