EXPRESSION OF MOLECULES ASSOCIATED WITH NEURONAL PLASTICITY IN THE STRIATUM AFTER ASPIRATION AND THERMOCOAGULATORY LESIONS OF THE CEREBRAL-CORTEX IN ADULT-RATS
Fg. Szele et al., EXPRESSION OF MOLECULES ASSOCIATED WITH NEURONAL PLASTICITY IN THE STRIATUM AFTER ASPIRATION AND THERMOCOAGULATORY LESIONS OF THE CEREBRAL-CORTEX IN ADULT-RATS, The Journal of neuroscience, 15(6), 1995, pp. 4429-4448
Like the hippocampus, the striatum receives excitatory afferents from
the cerebral cortex but, in the case of the striatum, very little is k
nown about the molecular events associated with plasticity after lesio
ns of this pathway, Using immunohistochemical techniques, we have exam
ined the effects of cortical lesions induced either by aspiration of t
he 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 aft
er aspiration but not after thermocoagulatory lesions, In contrast, sy
naptophysin, a marker of synaptic vesicles, remained unchanged in the
denervated striatum after both types of lesions. Immunostaining for ba
sic fibroblast growth factor (bFGF) markedly decreased in striatal ast
rocytes after both lesions, despite an increased staining for glial fi
brillary acidic protein (GFAP), The adhesion molecules tenascin, chond
roitin sulfate proteoglycans, highly polysialylated neural cell adhesi
on molecule (PSA-NCAM), and laminin did not change significantly in th
e 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 differe
nces 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 associ
ated with different types of pathology may differentially affect subco
rtical structures.