title: Absence of gliosis in a teleost model of spinal cord regeneration.
abstract: Among the cellular processes that follow injury to the central nervous system, glial scar formation is thought to be one of the major factors that prevent regeneration. In regeneration-competent organisms, glial scar formation has been a matter of controversy. We addressed this issue by examining the glial population after spinal cord injury in a model of regeneration competency, the knifefish Apteronotus leptorhynchus. Analysis of spinal cord sections immunostained against the glial markers glial fibrillary acidic protein, vimentin, or chondroitin sulfate proteoglycan failed to produce any evidence for the formation of a glial scar in the area of the lesion at post-injury survival times ranging from 5 to 185 days. This result was independent of the lesion paradigm applied-amputation of the caudal part of the spinal cord or hemisection lesioning-and similar after examination of transverse and longitudinal sections. We hypothesize that the well-developed network of radial glia in both the intact and the injured spinal cord provides a support system for regeneration of tissue lost to injury. This glial network is likely also involved in the generation of new cells, as indicated by the large subset of glial fibrillary acidic protein-labeled glia that express the stem cell marker Sox2.
authors.affiliation: Laboratory of Neurobiology, Department of Biology, Northeastern University, 134 Mugar Life Sciences, 360 Huntington Avenue, Boston, MA, 02115, USA.
authors.forename: Antonia G
authors.initials: AG
authors.lastname: Vitalo
authors.affiliation: Laboratory of Neurobiology, Department of Biology, Northeastern University, 134 Mugar Life Sciences, 360 Huntington Avenue, Boston, MA, 02115, USA.
authors.forename: Ruxandra F
authors.initials: RF
authors.lastname: Sîrbulescu
authors.affiliation: Laboratory of Neurobiology, Department of Biology, Northeastern University, 134 Mugar Life Sciences, 360 Huntington Avenue, Boston, MA, 02115, USA.
authors.forename: Iulian
authors.initials: I
authors.lastname: Ilieş
authors.affiliation: Laboratory of Neurobiology, Department of Biology, Northeastern University, 134 Mugar Life Sciences, 360 Huntington Avenue, Boston, MA, 02115, USA. g.zupanc@neu.edu.
authors.forename: Günther K H
authors.initials: GK
authors.lastname: Zupanc
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D029941:Fish Proteins / Q000378:metabolism; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D005911:Gliosis; D023702:Gymnotiformes / Q000502:physiology*; D007150:Immunohistochemistry; D018613:Microscopy, Confocal; D008856:Microscopy, Fluorescence; D058953:Neural Stem Cells / Q000473:pathology / Q000502:physiology; D009457:Neuroglia / Q000473:pathology / Q000502:physiology*; D055748:SOXB1 Transcription Factors / Q000378:metabolism; D013116:Spinal Cord / Q000473:pathology / Q000503:physiopathology; D013119:Spinal Cord Injuries / Q000473:pathology / Q000503:physiopathology*; D058630:Spinal Cord Regeneration / Q000502:physiology*
chemical_list: D029941:Fish Proteins; D005904:Glial Fibrillary Acidic Protein; D055748:SOXB1 Transcription Factors
keywords: Apteronotus leptorhynchus; Gliosis; Regeneration; Spinal cord injury; Teleost fish