Literature DB >> 17892412

Retrograde axonal degeneration "dieback" in the corticospinal tract after transection injury of the rat spinal cord: a confocal microscopy study.

Gamal I Seif1, Hiroshi Nomura, Charles H Tator.   

Abstract

Axonal dieback is a process in which axons in spinal tracts retract away from the initial site of injury. The purpose of this project is to study the dynamics of dieback in corticospinal tract (CST) axons after various time intervals post-injury, to find the optimal spatial-temporal window for regenerative treatment. Rats received transection injuries at the T8 spinal level and were sacrificed at different time periods (1, 2, 4, 8, and 16 weeks). Three weeks prior to sacrifice, DiI crystals were implanted in the sensorimotor cortex and produced excellent CST labeling, and clear delineation of the terminal bulbs of transected axons. With DiI and confocal microscopy, we visualized axons along the entire length of the CST, and quantified the temporal and spatial features of dieback in axons of the CST based on the location of the terminal bulbs. We found that the majority of axons stopped dieing back 4 weeks after injury by which time they were approximately 2.5 mm from the site of injury. However, at 8 and 16 weeks after injury, some terminal bulbs were more than 10 and 19 mm, respectively, from the site of injury.

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Year:  2007        PMID: 17892412     DOI: 10.1089/neu.2007.0323

Source DB:  PubMed          Journal:  J Neurotrauma        ISSN: 0897-7151            Impact factor:   5.269


  16 in total

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2.  Multipotent adult progenitor cells prevent macrophage-mediated axonal dieback and promote regrowth after spinal cord injury.

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Review 3.  Mitochondrial function in spinal cord injury and regeneration.

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Journal:  Cell Mol Life Sci       Date:  2022-04-13       Impact factor: 9.261

4.  The Ryk receptor is expressed in glial and fibronectin-expressing cells after spinal cord injury.

Authors:  Pau González; Carmen María Fernández-Martos; Ernest Arenas; Francisco Javier Rodríguez
Journal:  J Neurotrauma       Date:  2013-05-09       Impact factor: 5.269

5.  An ex vivo laser-induced spinal cord injury model to assess mechanisms of axonal degeneration in real-time.

Authors:  Starlyn L M Okada; Nicole S Stivers; Peter K Stys; David P Stirling
Journal:  J Vis Exp       Date:  2014-11-25       Impact factor: 1.355

6.  Another barrier to regeneration in the CNS: activated macrophages induce extensive retraction of dystrophic axons through direct physical interactions.

Authors:  Kevin P Horn; Sarah A Busch; Alicia L Hawthorne; Nico van Rooijen; Jerry Silver
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7.  Cortical PKC inhibition promotes axonal regeneration of the corticospinal tract and forelimb functional recovery after cervical dorsal spinal hemisection in adult rats.

Authors:  Xiaofei Wang; Jianguo Hu; Yun She; George M Smith; Xiao-Ming Xu
Journal:  Cereb Cortex       Date:  2013-06-28       Impact factor: 5.357

8.  Transgenic inhibition of astroglial NF-kappa B leads to increased axonal sparing and sprouting following spinal cord injury.

Authors:  Roberta Brambilla; Andres Hurtado; Trikaldarshi Persaud; Kim Esham; Damien D Pearse; Martin Oudega; John R Bethea
Journal:  J Neurochem       Date:  2009-05-26       Impact factor: 5.372

9.  Olig2-Induced Semaphorin Expression Drives Corticospinal Axon Retraction After Spinal Cord Injury.

Authors:  Masaki Ueno; Yuka Nakamura; Hiroshi Nakagawa; Jesse K Niehaus; Mari Maezawa; Zirong Gu; Atsushi Kumanogoh; Hirohide Takebayashi; Qing Richard Lu; Masahiko Takada; Yutaka Yoshida
Journal:  Cereb Cortex       Date:  2020-10-01       Impact factor: 5.357

10.  Synaptic elimination and protection after minimal injury depend on cell type and their prelesion structural dynamics in the adult cerebral cortex.

Authors:  A J Canty; L M Teles-Grilo Ruivo; C Nesarajah; S Song; J S Jackson; G E Little; V De Paola
Journal:  J Neurosci       Date:  2013-06-19       Impact factor: 6.167

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