Changes in [Ca2+](0) during anoxia in CNS white matter

IRREVERSIBLE anoxic injury of axons in the rat optic nerve requires the presence of extracellular Ca2+. To test the hypothesis that Ca2+ enters an intracellular compartment during anoxia we monitored [Ca2+](0) in this CNS white matter tract using ion-sensitive microelectrodes. Periods of anoxia lasting 15 min resulted in a rapid, reversible increase in [Ca2+](0) accompanied by transient loss of nerve conduction. This increase in [Ca2+](0) was apparently the result of extracellular space shrinkage. Anoxic periods lasting 60 min resulted in an initial rise followed by a sustained fall in [Ca2+](0), indicative of net influx of Ca2+ into an intracellular compartment. Following reoxygenation after 60 min of anoxia, [Ca2+](0) slowly returned toward control levels but nerve conduction recovered incompletely, indicating irreversible loss of function. Removal of bath Ca2+ lowered [Ca2+](0) to about 100 mu M, prevented the anoxia-induced fall in [Ca2+](0), and protected against irreversible loss of the compound action potential. (C) 1998 Rapid Science Ltd.