title: Fate of severed cortical projection axons.
abstract: Corticospinal neurons show a primarily degenerative response to axotomy in adult mammals. The long remaining proximal axon with its extensive synaptic contacts may contribute to the lack of initial regenerative response in this cell type. We examined a related group of cortical axons after lesions in the subcortical white matter close to their cell bodies of origin. With cholera B chain conjugated to horseradish peroxidase (CTB-HRP), transcallosal axons projecting into areas of a lesion were labeled. Animals surviving between 2 days and 4 months were examined with both light microscopic and ultrastructural techniques. During the first several days after injury, many of the axon terminals projecting into the lesion site had the appearance of axonal sprouts, although the majority of endings had the appearance of degenerating terminal swellings. By 2 weeks after injury some axonal sprouts had extended a short distance along the margins of the lesions, into overlying cortex. Four weeks after injury there is a reduction in the number of axons extending toward the lesion. This loss of axons appeared progressive and resulted in not only a loss of labeled axons, but also eventually in atrophy of the subcortical white matter near the lesion. In comparison to corticospinal axon lesions in the spinal cord or medullary pyramids, there is more extensive axonal sprouting and elongation after subcortical lesions. Degenerative morphological features still predominate after subcortical lesions and no successful trans-lesion axonal regeneration occurs. Axonal retraction and loss are both accelerated and more extensive after proximal subcortical axotomy than after corticospinal tract lesions.
authors.affiliation: Department of Neurology, University of Maryland School of Medicine, Baltimore.
authors.forename: P S
authors.initials: PS
authors.lastname: Fishman
authors.forename: A
authors.initials: A
authors.lastname: Mattu
mesh_terms: D000818:Animals; D001369:Axons / Q000502:physiology* / Q000648:ultrastructure; D002540:Cerebral Cortex / Q000166:cytology* / Q000502:physiology / Q000648:ultrastructure; D002772:Cholera Toxin; D006651:Histocytochemistry; D006735:Horseradish Peroxidase; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009410:Nerve Degeneration / Q000502:physiology; D009411:Nerve Endings / Q000648:ultrastructure; D009416:Nerve Regeneration; D009434:Neural Pathways / Q000166:cytology / Q000502:physiology / Q000648:ultrastructure; D017966:Pyramidal Cells / Q000502:physiology / Q000648:ultrastructure; D013116:Spinal Cord / Q000166:cytology* / Q000502:physiology / Q000648:ultrastructure
chemical_list: C052635:cholera toxin, B subunit-horseradish peroxidase; D002772:Cholera Toxin; D006735:Horseradish Peroxidase