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The Journal of Neurophysiology Vol. 84 No. 2 August 2000, pp. 1116-1119
Copyright ©2000 by the American Physiological Society
RAPID COMMUNICATION
Loeb Health Research Institute, Ottawa Hospital
Civic Campus,
University of Ottawa, Ottawa, Ontario K1Y 4K9, Canada
Li, Shuxin,
Qiubo Jiang, and
Peter K. Stys.
Important Role of Reverse Na+-Ca2+
Exchange in Spinal Cord White Matter Injury at Physiological
Temperature. J. Neurophysiol. 84: 1116-1119, 2000. 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.
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