PMID- 24361176
OWN - NLM
STAT- MEDLINE
DCOM- 20140925
LR  - 20220309
IS  - 1873-7544 (Electronic)
IS  - 0306-4522 (Linking)
VI  - 260
DP  - 2014 Feb 28
TI  - A characterization of white matter pathology following spinal cord compression 
      injury in the rat.
PG  - 227-39
LID - S0306-4522(13)01040-3 [pii]
LID - 10.1016/j.neuroscience.2013.12.024 [doi]
AB  - Our laboratory has previously described the characteristics of neuronal injury in 
      a rat compression model of spinal cord injury (SCI), focussing on the impact of 
      this injury on the gray matter. However, white matter damage is known to play a 
      critical role in functional outcome following injury. Therefore, in the present 
      study, we used immunohistochemistry and electron microscopy to examine the 
      alterations to the white matter that are initiated by compression SCI applied at 
      T12 vertebral level. A significant loss of axonal and dendritic cytoskeletal 
      proteins was observed at the injury epicenter within 1day of injury. This was 
      accompanied by axonal dysfunction, as demonstrated by the accumulation of 
      beta-amyloid precursor protein (beta-APP), with a peak at 3days post-SCI. A similar, 
      acute loss of cytoskeletal proteins was observed up to 5mm away from the injury 
      epicenter and was particularly evident rostral to the lesion site, whereas beta-APP 
      accumulation was prominent in tracts proximal to the injury. Early myelin loss 
      was confirmed by myelin basic protein (MBP) immunostaining and by electron 
      microscopy, which also highlighted the infiltration of inflammatory and red blood 
      cells. However, 6weeks after injury, areas of new Schwann cell and 
      oligodendrocyte myelination were observed. This study demonstrates that 
      substantial white matter damage occurs following compression SCI in the rat. 
      Moreover, the loss of cytoskeletal proteins and accumulation of beta-APP up to 5mm 
      away from the lesion site within 1day of injury indicates the rapid manner in 
      which the axonal damage extends in the rostro-caudal axis. This is likely due to 
      both Wallerian degeneration and spread of secondary cell death, with the latter 
      affecting axons both proximal and distal to the injury.
CI  - Copyright (c) 2013 IBRO. Published by Elsevier Ltd. All rights reserved.
FAU - Ward, R E
AU  - Ward RE
AD  - Centre for Neuroscience and Trauma, Blizard Institute, Barts and The London 
      School of Medicine and Dentistry, Queen Mary University of London, London E1 2AT, 
      UK. Electronic address: emailrache@yahoo.co.uk.
FAU - Huang, W
AU  - Huang W
AD  - Centre for Neuroscience and Trauma, Blizard Institute, Barts and The London 
      School of Medicine and Dentistry, Queen Mary University of London, London E1 2AT, 
      UK; The Institute of Medical Sciences, School of Medical Science, University of 
      Aberdeen, Foresterhill, Aberdeen AB25 2ZD, UK.
FAU - Kostusiak, M
AU  - Kostusiak M
AD  - Centre for Neuroscience and Trauma, Blizard Institute, Barts and The London 
      School of Medicine and Dentistry, Queen Mary University of London, London E1 2AT, 
      UK.
FAU - Pallier, P N
AU  - Pallier PN
AD  - Centre for Neuroscience and Trauma, Blizard Institute, Barts and The London 
      School of Medicine and Dentistry, Queen Mary University of London, London E1 2AT, 
      UK.
FAU - Michael-Titus, A T
AU  - Michael-Titus AT
AD  - Centre for Neuroscience and Trauma, Blizard Institute, Barts and The London 
      School of Medicine and Dentistry, Queen Mary University of London, London E1 2AT, 
      UK.
FAU - Priestley, J V
AU  - Priestley JV
AD  - Centre for Neuroscience and Trauma, Blizard Institute, Barts and The London 
      School of Medicine and Dentistry, Queen Mary University of London, London E1 2AT, 
      UK.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20131217
PL  - United States
TA  - Neuroscience
JT  - Neuroscience
JID - 7605074
RN  - 0 (Neurofilament Proteins)
SB  - IM
MH  - Animals
MH  - Female
MH  - Nerve Fibers, Myelinated/*ultrastructure
MH  - Neurofilament Proteins/metabolism
MH  - Neurons/metabolism/ultrastructure
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Spinal Cord Compression/*pathology
MH  - Thoracic Vertebrae
OTO - NOTNLM
OT  - CST
OT  - DC
OT  - DLWM
OT  - FITC
OT  - IR
OT  - MAP-2
OT  - MBP
OT  - NF-200
OT  - PB
OT  - PBS
OT  - PFA
OT  - PO
OT  - SCI
OT  - TRITC
OT  - VLWM
OT  - VWM
OT  - axons
OT  - compression injury
OT  - corticospinal tract
OT  - demyelination
OT  - dorsal column
OT  - dorsolateral white matter
OT  - fluorescein isothiocyanate
OT  - immunoreactivity
OT  - microtubule associated protein-2
OT  - myelin basic protein
OT  - neurofilament
OT  - neurofilament-200
OT  - paraformaldehyde
OT  - phosphate buffer
OT  - phosphate-buffered saline
OT  - propylene oxide
OT  - spinal cord injury
OT  - tetramethylrhodamine isothiocyanate
OT  - ventral white matter
OT  - ventrolateral white matter
OT  - white matter
OT  - beta-APP
OT  - beta-amyloid precursor protein
EDAT- 2013/12/24 06:00
MHDA- 2014/09/26 06:00
CRDT- 2013/12/24 06:00
PHST- 2013/07/09 00:00 [received]
PHST- 2013/12/09 00:00 [revised]
PHST- 2013/12/09 00:00 [accepted]
PHST- 2013/12/24 06:00 [entrez]
PHST- 2013/12/24 06:00 [pubmed]
PHST- 2014/09/26 06:00 [medline]
AID - S0306-4522(13)01040-3 [pii]
AID - 10.1016/j.neuroscience.2013.12.024 [doi]
PST - ppublish
SO  - Neuroscience. 2014 Feb 28;260:227-39. doi: 10.1016/j.neuroscience.2013.12.024. 
      Epub 2013 Dec 17.