Ultrastructural evidence for differential axonal sprouting in the striatumafter thermocoagulatory and aspiration lesions of the cerebral cortex in adult rats
K. Uryu et al., Ultrastructural evidence for differential axonal sprouting in the striatumafter thermocoagulatory and aspiration lesions of the cerebral cortex in adult rats, NEUROSCIENC, 105(2), 2001, pp. 307-316
Thermocoagulation of pial blood vessels overlying the cerebral cortex induc
es an ischemic degeneration of the cortex. We have previously shown with an
atomical tracing techniques that thermocoagulatory lesions of le sensorimot
or cortex trigger a robust axonal sprouting of contralateral cortical neuro
ns into the denervated striatum. Similar sprouting was not observed after a
cute aspiration lesions of the same cortical region. We have now examined i
mmunostaining for the growth-associated protein (GAP)-43 at the ultrastruct
ural level after both types of lesions. A modest increase in growth cone-li
ke structures was observed just below the corpus callosum after both lesion
s. However, GAP-43-positive growth cone-like structures were markedly incre
ased in the denervated dorsolateral striatum only after thermocoagulatory l
esions. In contrast, no significant increase in growth cone immunostaining
was found in the dorsolateral striatum after aspiration lesions, confirming
the absence of axonal sprouting in the dorsolateral striatum in this condi
tion. Corticostriatal inputs make asymmetric synapses with dendritic spines
of striatal neurons. As expected, the density of asymmetric synapses was m
arkedly decreased in the dorsolateral striatum after aspiration lesions. Ho
wever, it was not different from control after thermocoagulatory lesions th
at removed the same cortical area. The density of symmetric synapses was de
creased after both types of lesions at 16 but not 42 days post-surgery.
These data reveal that robust axonal and synaptic remodeling can occur in t
he dorsolateral striatum of adult rats after ischemic lesions of the cerebr
al cortex and further demonstrate marked differences in the degree of anato
mical plasticity induced by two different types of cortical lesions. (C) 20
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