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 microM, prevented the anoxia-induced fall in [Ca2+]0, and protected against irreversible loss of the compound action potential.
Department of Neurology, University of Washington School of Medicine, Seattle 98195, USA.
A M
AM
Brown
R
R
Fern
J P
JP
Jarvinen
K
K
Kaila
B R
BR
Ransom
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002138:Calibration; D002490:Central Nervous System / Q000378:metabolism*; D004594:Electrophysiology; D002534:Hypoxia, Brain / Q000378:metabolism*; D008839:Microelectrodes; D009900:Optic Nerve / Q000378:metabolism; D051381:Rats
D002118:Calcium