title: Ultrastructural evidence for differential axonal sprouting in the striatum after thermocoagulatory and aspiration lesions of the cerebral cortex in adult rats.
abstract: Thermocoagulation of pial blood vessels overlying the cerebral cortex induces an ischemic degeneration of the cortex. We have previously shown with anatomical tracing techniques that thermocoagulatory lesions of the sensorimotor cortex trigger a robust axonal sprouting of contralateral cortical neurons into the denervated striatum. Similar sprouting was not observed after acute aspiration lesions of the same cortical region. We have now examined immunostaining for the growth-associated protein (GAP)-43 at the ultrastructural level after both types of lesions. A modest increase in growth cone-like structures was observed just below the corpus callosum after both lesions. However, GAP-43-positive growth cone-like structures were markedly increased in the denervated dorsolateral striatum only after thermocoagulatory lesions. 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 condition. Corticostriatal inputs make asymmetric synapses with dendritic spines of striatal neurons. As expected, the density of asymmetric synapses was markedly decreased in the dorsolateral striatum after aspiration lesions. However, it was not different from control after thermocoagulatory lesions that removed the same cortical area. The density of symmetric synapses was decreased 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 the dorsolateral striatum of adult rats after ischemic lesions of the cerebral cortex and further demonstrate marked differences in the degree of anatomical plasticity induced by two different types of cortical lesions.
authors.affiliation: Department of Pharmacology, University of Pennsylvania, Philadelphia, USA.
authors.forename: K
authors.initials: K
authors.lastname: Uryu
authors.forename: L
authors.initials: L
authors.lastname: MacKenzie
authors.forename: M F
authors.initials: MF
authors.lastname: Chesselet
mesh_terms: D000818:Animals; D002452:Cell Count; D002540:Cerebral Cortex / Q000293:injuries* / Q000378:metabolism / Q000648:ultrastructure; D003337:Corpus Callosum / Q000293:injuries / Q000378:metabolism / Q000648:ultrastructure; D003712:Dendrites / Q000378:metabolism / Q000648:ultrastructure; D003714:Denervation / Q000379:methods; D004564:Electrocoagulation / Q000009:adverse effects*; D019922:GAP-43 Protein / Q000378:metabolism; D020439:Growth Cones / Q000378:metabolism / Q000648:ultrastructure*; D007150:Immunohistochemistry; D008297:Male; D008854:Microscopy, Electron; D017072:Neostriatum / Q000378:metabolism / Q000648:ultrastructure*; D009416:Nerve Regeneration / Q000502:physiology*; D009473:Neuronal Plasticity / Q000502:physiology*; D017729:Presynaptic Terminals / Q000378:metabolism / Q000648:ultrastructure*; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D019922:GAP-43 Protein