title: Repair of the transected spinal cord at different stages of development in the North American opossum, Didelphis virginiana.
abstract: When the thoracic spinal cord is transected on postnatal day (PD) 5 in the North American opossum, descending and ascending axons grow through the lesion site. When the lesion is made on PD20, comparable growth is limited to a subset of descending axons. To better understand the mechanisms underlying these differences, we analyzed the transection site at different times after lesioning at both ages. Axons which crossed the lesion site could be identified using silver impregnation and immunostaining for neurofilament. Nissl stains revealed that abnormal appearing grey matter was also present in some of the PD5 cases. In many PD5 cases, however, and in all of the animals transected at PD20, grey matter was not present at the lesion site. Immunostaining with a neuron specific antibody supported that conclusion. However, immunostaining with phenotypic specific antibodies revealed that glial cells were present in all cases. Immunostaining for Schwann cells was negative. Fibronectin-positive cells were also present at the lesion site after transection of the thoracic cord at PD20, but their identity was uncertain. When injections of bromodeoxyuridine (BrdU), a thymidine analog, were made at different times after lesioning and the pups were sacrificed for BrdU immunohistochemistry up to 40 days later, labeled cells were found in the tissue which bridged the lesion site indicating that cell proliferation contributed to reconstruction at the lesion site.
authors.affiliation: Department of Anatomy and Medical Education, The Ohio State University, College of Medicine, Columbus, OH, USA. jterman@jhmi.edu
authors.forename: J R
authors.initials: JR
authors.lastname: Terman
authors.forename: X M
authors.initials: XM
authors.lastname: Wang
authors.forename: G F
authors.initials: GF
authors.lastname: Martin
mesh_terms: D000367:Age Factors; D000818:Animals; D001369:Axons / Q000378:metabolism / Q000648:ultrastructure*; D019771:Axotomy / Q000009:adverse effects; D002455:Cell Division / Q000502:physiology; D004525:Efferent Pathways / Q000166:cytology / Q000254:growth & development* / Q000293:injuries; D005353:Fibronectins / Q000378:metabolism; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D007150:Immunohistochemistry; D008869:Microtubule-Associated Proteins / Q000378:metabolism; D009416:Nerve Regeneration / Q000502:physiology*; D016900:Neurofilament Proteins / Q000378:metabolism; D009457:Neuroglia / Q000166:cytology / Q000378:metabolism; D009473:Neuronal Plasticity / Q000502:physiology*; D009893:Opossums / Q000033:anatomy & histology / Q000254:growth & development* / Q000293:injuries; D012583:Schwann Cells / Q000166:cytology / Q000378:metabolism; D013116:Spinal Cord / Q000166:cytology / Q000254:growth & development* / Q000378:metabolism; D013119:Spinal Cord Injuries / Q000473:pathology / Q000503:physiopathology*; D013904:Thoracic Vertebrae
chemical_list: D005353:Fibronectins; D005904:Glial Fibrillary Acidic Protein; D008869:Microtubule-Associated Proteins; D016900:Neurofilament Proteins