Expression of the neural adhesion molecule L1 and its potential involv
ement in axonal sprouting were examined in the deafferented rat dentat
e gyrus. We focused on the dentate gyrus because of its well-defined c
ytoarchitecture and well-characterized neuronal degeneration and sprou
ting response following entorhinal cortex lesions. In the molecular la
yer of the dentate gyrus, a trilaminar staining pattern was observed,
with the middle molecular layer exhibiting slightly denser immunolabel
ing compared to both inner and outer molecular layers. Two to 12 days
after a unilateral entorhinal cortex lesion, a progressive loss of L1
immunolabeling was noted in the ipsilateral middle and outer molecular
layers, followed by a substantial reappearance of immunostaining 65 d
ays after lesion incidence. The width of the immunostained ipsilateral
inner molecular layer revealed a progressive widening and by postlesi
on day 65 occupied about 50% of the total width of the molecular layer
. Immunoelectron microscopy localized L1 to the surface of unmyelinate
d axons in both normal and deafferented dentate gyrus. In situ hybridi
zation revealed LI messenger RNA confined to neurons throughout the hi
ppocampal formation, but did not indicate changes in L1 messenger RNA
levels in the hippocampus, dentate gyrus, entorhinal cortex or basal f
orebrain in response to unilateral entorhinal cortex lesions. Changes
in L1 immunolabeling in the deafferented dentate gyrus corresponded in
a spatial and temporal manner to changes of the synaptic marker synap
tophysin and axonal marker phosphorylated tau. Results of the present
study are most consistent with the view that L1 is expressed on reinne
rvating fibers after they make synaptic contacts with other structures
. Thus, L1 appears to be involved in the maturation and stabilization
of reinnervating fibers and consequently may play an important role in
the repair process of the lesioned adult CNS. Copyright (C) 1996 IBRO
.