title: Is Remodelling of Corticospinal Tract Terminations Originating in the Intact Hemisphere Associated with Recovery following Transient Ischaemic Stroke in the Rat?
abstract: Following large strokes that encompass the cerebral cortex, it has been suggested that the corticospinal tract originating from the non-ischaemic hemisphere reorganises its pattern of terminal arborisation within the spinal cord to compensate for loss of function. However many strokes in humans predominantly affect subcortical structures with minimal involvement of the cerebral cortex. The aim of the present study was to determine whether remodelling of corticospinal terminals arising from the non-ischaemic hemisphere was associated with spontaneous recovery in rats with subcortical infarcts. Rats were subjected to transient middle cerebral artery occlusion or sham surgery and 28 days later, when animals exhibited functional recovery, cholera toxin b subunit was injected into the contralesional, intact forelimb motor cortex in order to anterogradely label terminals within cervical spinal cord segments. Infarcts were limited to subcortical structures and resulted in partial loss of corticospinal tract axons from the ischaemic hemisphere. Quantitative analysis revealed there was no significant difference in the numbers of terminals on the contralesional side of the spinal grey matter between ischaemic and sham rats. The results indicate that significant remodelling of the corticospinal tract from the non-ischaemic hemisphere is not associated with functional recovery in animals with subcortical infarcts.
authors.affiliation: Institute of Neuroscience and Psychology, College of Medicine, Veterinary Medicine and Life Sciences, University of Glasgow, Glasgow, United Kingdom.
authors.forename: Emma J
authors.initials: EJ
authors.lastname: Mitchell
authors.affiliation: Institute of Neuroscience and Psychology, College of Medicine, Veterinary Medicine and Life Sciences, University of Glasgow, Glasgow, United Kingdom.
authors.forename: Deborah
authors.initials: D
authors.lastname: Dewar
authors.affiliation: Institute of Neuroscience and Psychology, College of Medicine, Veterinary Medicine and Life Sciences, University of Glasgow, Glasgow, United Kingdom.
authors.forename: David J
authors.initials: DJ
authors.lastname: Maxwell
mesh_terms: D000818:Animals; D001369:Axons / Q000473:pathology; D004195:Disease Models, Animal; D005552:Forelimb / Q000503:physiopathology; D066128:Gray Matter; D006801:Humans; D020244:Infarction, Middle Cerebral Artery; D008297:Male; D009044:Motor Cortex / Q000503:physiopathology*; D009416:Nerve Regeneration; D009473:Neuronal Plasticity; D011712:Pyramidal Tracts / Q000503:physiopathology* / Q000601:surgery; D051381:Rats; D020127:Recovery of Function; D013116:Spinal Cord / Q000503:physiopathology* / Q000601:surgery; D020521:Stroke / Q000503:physiopathology* / Q000601:surgery