scholarly journals MultiexponentialT2, magnetization transfer, and quantitative histology in white matter tracts of rat spinal cord

2010 ◽  
Vol 63 (4) ◽  
pp. 902-909 ◽  
Author(s):  
Adrienne N. Dula ◽  
Daniel F. Gochberg ◽  
Holly L. Valentine ◽  
William M. Valentine ◽  
Mark D. Does
Keyword(s):  
Spinal Cord ◽  
White Matter ◽  
Magnetization Transfer ◽  
Rat Spinal Cord ◽  
White Matter Tracts ◽  
Quantitative Histology

scholarly journals In vivo DTI evaluation of white matter tracts in rat spinal cord

2006 ◽  
Vol 24 (1) ◽  
pp. 231-234 ◽  
Author(s):  
Jayaroop Gullapalli ◽  
Jaroslaw Krejza ◽  
Eric D. Schwartz
Keyword(s):  
Spinal Cord ◽  
White Matter ◽  
Rat Spinal Cord ◽  
White Matter Tracts

scholarly journals Important Role of Reverse Na+-Ca2+Exchange in Spinal Cord White Matter Injury at Physiological Temperature

2000 ◽  
Vol 84 (2) ◽  
pp. 1116-1119 ◽  
Author(s):  
Shuxin Li ◽  
Qiubo Jiang ◽  
Peter K. Stys
Keyword(s):  
Spinal Cord ◽  
White Matter ◽  
Traumatic Injury ◽  
White Matter Injury ◽  
Mechanical Trauma ◽  
White Matter Tracts ◽  
Physiological Temperature ◽  
Cord Injury ◽  
Cellular Ca

Spinal cord injury is a devastating condition in which most of the clinical disability results from dysfunction of white matter tracts. Excessive cellular Ca2+ accumulation is a common phenomenon after anoxia/ischemia or mechanical trauma to white matter, leading to irreversible injury because of overactivation of multiple Ca2+-dependent biochemical pathways. In the present study, we examined the role of Na+-Ca2+ exchange, a ubiquitous Ca2+ transport mechanism, in anoxic and traumatic injury to rat spinal dorsal columns in vitro. Excised tissue was maintained in a recording chamber at 37°C and injured by exposure to an anoxic atmosphere for 60 min or locally compressed with a force of 2 g for 15 s. Mean compound action potential amplitude recovered to ≈25% of control after anoxia and to ≈30% after trauma. Inhibitors of Na+-Ca2+ exchange (50 μM bepridil or 10 μM KB-R7943) improved functional recovery to ≈60% after anoxia and ≈70% after traumatic compression. These inhibitors also prevented the increase in calpain-mediated spectrin breakdown products induced by anoxia. We conclude that, at physiological temperature, reverse Na+-Ca2+exchange plays an important role in cellular Ca2+ overload and irreversible damage after anoxic and traumatic injury to dorsal column white matter tracts.

Delayed Glial Cell Death Following Wallerian Degeneration in White Matter Tracts after Spinal Cord Dorsal Column Cordotomy in Adult Rats

2001 ◽  
Vol 168 (2) ◽  
pp. 213-224 ◽  
Author(s):  
Patricia Warden ◽  
Norman I. Bamber ◽  
Huaying Li ◽  
Andrew Esposito ◽  
Kaashif A. Ahmad ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Cell Death ◽  
White Matter ◽  
Glial Cell ◽  
Wallerian Degeneration ◽  
Dorsal Column ◽  
Adult Rats ◽  
White Matter Tracts ◽  
Spinal Cord Dorsal

scholarly journals Upregulation of EphA Receptor Expression in the Injured Adult Rat Spinal Cord

2002 ◽  
Vol 11 (3) ◽  
pp. 229-239 ◽  
Author(s):  
Christopher A. Willson ◽  
Margarita Irizarry-Ramírez ◽  
Hope E. Gaskins ◽  
Lillian Cruz-Orengo ◽  
Johnny D. Figueroa ◽  
...  
Keyword(s):  
Spinal Cord ◽  
White Matter ◽  
Gray Matter ◽  
Receptor Expression ◽  
Axonal Guidance ◽  
Receptor Subtypes ◽  
Rat Spinal Cord ◽  
Functional Connections ◽  
Cord Injury ◽  
Epha Receptor

After spinal cord injury (SCI), the inability of supraspinal neurons to regenerate or reform functional connections is likely due to proteins in the surrounding microenvironment restricting regeneration. EphAs are a family of receptor tyrosine kinases that are involved in axonal guidance during development. These receptors and their ligands, the Ephrins, act via repulsive mechanisms to guide growing axons towards their appropriate targets and allow for the correct developmental connections to be made. In the present study, we investigated whether EphA receptor expression changed after a thoracic contusion SCI. Our results indicate that several EphA molecules are upregulated after SCI. Using semiquantitative RT-PCR to investigate mRNA expression after SCI, we found that EphA3, A4, and A7 mRNAs were upregulated. EphA3, A4, A6, and A8 receptor immunoreactivity increased in the ventrolateral white matter (VWM) at the injury epicenter. EphA7 had the highest level of immunoreactivity in both control and injured rat spinal cord. EphA receptor expression in the white matter originated from glial cells as coexpression in both astrocytes and oligodendrocytes was observed. In contrast, gray matter expression was localized to neurons of the ventral gray matter (motor neurons) and dorsal horn. After SCI, specific EphA receptor subtypes are upregulated and these increases may create an environment that is unfavorable for neurite outgrowth and functional regeneration.

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