Resistance of isolated mammalian spinal cord white matter to oxygen-glucose deprivation

We found that isolated guinea pigspinal cord white matter is resistant to acute oxygen-glucosedeprivation. Sixty minutes of oxygen-glucose deprivation resulted in a60% reduction of compound action potential (CAP) conductance, andthere was a near complete recovery after 60 min reperfusion.Corresponding horseradish peroxidase-exclusion assay showed littleaxonal membrane damage. To further deprive the axons of metabolicsubstrate, we added 2 mM sodium cyanide or 2 mM sodium azide, bothmitochondrial suppressors, to the ischemic medium, whichcompletely abolished CAP and resulted in a 15 to ~30% recoverypostreperfusion. Both compounds preferentially reduced the conductanceof large diameter axons. We suggest the residual ATP in ourischemic model can protect anatomic integrity and physiological functioning of spinal axons following ischemic insult. Thisfurther suggests that oxygen-glucose deprivation alone cannot be solely responsible for short-term functional and anatomic damage. The damagingeffects 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.