mammalian spinal cord white matter to oxygen-glucose de-

We found that isolated guinea pig spinal cord white matter is resistant to acute oxygen-glucose deprivation. Sixty minutes of oxygen-glucose deprivation resulted in a 60 % reduction of compound action potential (CAP) conductance, and there was a near complete recovery after 60 min reperfusion. Corre-sponding horseradish peroxidase-exclusion assay showed lit-tle axonal membrane damage. To further deprive the axons of metabolic substrate, we added 2 mM sodium cyanide or 2 mM sodium azide, both mitochondrial suppressors, to the ischemic medium, which completely abolished CAP and re-sulted in a 15 to 30 % recovery postreperfusion. Both com-pounds preferentially reduced the conductance of large diam-eter axons. We suggest the residual ATP in our ischemic model can protect anatomic integrity and physiological func-tioning of spinal axons following ischemic insult. This further suggests that oxygen-glucose deprivation alone cannot be solely responsible for short-term functional and anatomic 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. axons; neurotrauma; reperfusion; mitochondria; membrane OXYGEN-GLUCOSE DEPRIVATION, or ischemia, can produce or exacerbate many devastating insults to the central nervous system (CNS), such as stroke and paralysis (1, 21, 29, 31, 35, 36). In the case of spinal cord injury, paralysis can be a consequence of even brief ischemic episodes such as result from clamping of the aorta during life-saving surgeries (1, 7, 12, 13, 19). Further-more, ischemia can arise secondary to physical insults when the integrity of blood vessels is compromised (20, 35, 36). Altogether, it is widely recognized that ische-mia plays a critical role in the neuropathology of the CNS in general and the spinal cord in particular (20