Journal of Neuroscience, Vol 15, 4429-4448, Copyright © 1995 by Society for Neuroscience
Expression of molecules associated with neuronal plasticity in the striatum after aspiration and thermocoagulatory lesions of the cerebral cortex in adult rats
FG Szele, C Alexander and MF Chesselet
Department of Pharmacology, University of Pennsylvania, Philadelphia 19104, USA.
Like the hippocampus, the striatum receives excitatory afferents from the
cerebral cortex but, in the case of the striatum, very little is known
about the molecular events associated with plasticity after lesions of this
pathway. Using immunohistochemical techniques, we have examined the effects
of cortical lesions induced either by aspiration of the frontoparietal
cortex or by thermocoagulation of pial blood vessels on axonal and glial
molecules associated with neuronal plasticity in the striatum. The growth
associated protein GAP-43, a molecule present in axons and growth cones,
decreased in the dorsolateral striatum after aspiration but not after
thermocoagulatory lesions. In contrast, synaptophysin, a marker of synaptic
vesicles, remained unchanged in the denervated striatum after both types of
lesions. Immunostaining for basic fibroblast growth factor (bFGF) markedly
decreased in striatal astrocytes after both lesions, despite an increased
staining for glial fibrillary acidic protein (GFAP). The adhesion molecules
tenascin, chondroitin sulfate proteoglycans, highly polysialylated neural
cell adhesion molecule (PSA-NCAM), and laminin did not change significantly
in the gray matter of the dorsolateral striatum after either type of
lesion. These effects differed from those observed after partial
denervation of the hippocampus and spinal cord, revealing marked regional
differences in the response of axonal and glial proteins to afferent
lesions. In addition, the results further indicate that cortical lesions
have both similar and distinct consequences, depending on the procedure by
which the lesions are induced, suggesting that cortical lesions associated
with different types of pathology may differentially affect subcortical
structures.
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