CHANGES IN [CA2-MATTER(](0) DURING ANOXIA IN CNS WHITE)

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