Ak. Butler et al., REGULATION OF THE POLYSIALYLATED FORM OF THE NEURAL CELL-ADHESION MOLECULE IN THE DEVELOPING STRIATUM - EFFECTS OF CORTICAL-LESIONS, Journal of comparative neurology, 389(2), 1997, pp. 289-308
Early in development, the polysialylated form of the neural cell adhes
ion molecule (PSA-NCAM) is expressed by growth cones; neuronal process
es, and neuronal cell bodies. In rat striatum, PSA-NCAM expression bec
omes progressively restricted to pre-and postsynaptic membranes and is
undetectable by postnatal day 25 (P25), i.e., after corticostriatal s
ynaptogenesis. This study examined the effects of cortical lesions per
formed on P14, when the corticostriatal projection is already primaril
y unilateral and cortical inputs have not yet formed asymmetric synaps
es on striatal neurons. Rats were killed on P25, and PSA-NCAM expressi
on was examined by immunoblotting and immunohistochemistry with light
and electron microscopy. In contrast to the case in controls, PSA-NCAM
expression was maintained in the striatum of lesioned pups. Ultrastru
ctural studies showed that PSA-NCAM was present 1) in growth cone-like
structures and neuronal processes and 2) in striatal neurons. Togethe
r with the presence of growth cones, the observation that the number o
f asymmetric synapses was unchanged in the denervated striatum suggest
s that axonal sprouting occurred in response to the lesion. This was c
onfirmed by axonal labeling in the denervated striatum after injection
of Fluoro-Ruby in the contralateral cortex. The data indicate that P1
4 cortical lesions affect PSA-NCAM expression in the developing striat
um 1) by inducing a robust axonal plasticity resulting in the presence
of immature presynaptic elements that contain PSA-NCAM and 2) by dela
ying the loss of PSA-NCAM expression in striatal neurons, suggesting t
hat the lesion affects the time course of striatal maturation. (C) 199
7 Wiley-liss, Inc.