REGULATION OF THE POLYSIALYLATED FORM OF THE NEURAL CELL-ADHESION MOLECULE IN THE DEVELOPING STRIATUM - EFFECTS OF CORTICAL-LESIONS

Citation
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
Citations number
78
ISSN journal
00219967
Volume
389
Issue
2
Year of publication
1997
Pages
289 - 308
Database
ISI
SICI code
0021-9967(1997)389:2<289:ROTPFO>2.0.ZU;2-W
Abstract
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.