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Am J Physiol Cell Physiol (May 22, 2002). doi:10.1152/ajpcell.00591.2001
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Articles in PresS, published online ahead of print May 22, 2002
Am J Physiol Cell Physiol, 10.1152/ajpcell.00591.2001
Submitted on December 20, 2001
Accepted on May 15, 2002

The Resistance of Isolated Mammalian Spinal Cord White Matter to Oxygen-Glucose Deprivation

Melissa A. Peasley1 and Riyi Shi1*

1 Basic Medical Sciences, Purdue University, West Lafayette, IN, USA

* To whom correspondence should be addressed. E-mail: riyi{at}purdue.edu.

We found that isolated guinea pig spinal cord white matter is resistant to acute oxygen-glucose deprivation. Sixty minutes oxygen-glucose deprivation resulted in a 60% reduction of compound action potential (CAP) conductance, and a near complete recovery following 60 minutes reperfusion. Corresponding horseradish peroxidase-exclusion assay showed little axonal membrane damage. To further deprive the axons of metabolic substrate, 2 mM sodium cyanide or 2 mM sodium azide, both mitochondrial suppressors, were added to the ischemic medium, which completely abolished CAP and resulted in a 15~30% recovery post-reperfusion. Both compounds preferentially reduced the conductance of large diameter axons. We suggest the residual ATP in our ischemic model can protect anatomical integrity and physiological functioning of spinal axons following ischemic insult. This further suggests that oxygen-glucose deprivation alone cannot be solely responsible for short-term functional and anatomical damage. The damaging effects of ischemia in vivo may be mediated by factors originating from the gray matter of the cord or other systemic factors, both were largely eliminated in our in vitro white matter preparation.




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