Ransom B R, Waxman S G, Davis P K
Department of Neurology, Yale University School of Medicine, New Haven, CT 06510.
Neurology. 1990 Sep;40(9):1399-403. doi: 10.1212/wnl.40.9.1399.
Gray and white matter of the mammalian CNS are both damaged by anoxia. Anoxic injury in gray matter is mediated in part by excessive accumulation of excitotoxins like glutamate. Drugs such as ketamine, a dissociative anesthetic known to block glutamate (NMDA) receptors, reduce hypoxic neuronal injury in gray matter. In this study we used the isolated rat optic nerve preparation to determine if ketamine influences recovery after anoxia in a nonsynaptic system, ie, CNS white matter. Optic nerves from adult rats were exposed to a standard 60-minute period of anoxia. Ketamine (1 mM) improved recovery of the compound action potential (CAP) after anoxia. Since glutamate and aspartate (up to 10 mM) had no effect on CAP amplitude in the optic nerve, the effect of ketamine is probably not mediated by NMDA receptor blockade. These observations indicate that ketamine is able to protect CNS white matter, as well as gray matter, from anoxic injury.
