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

AM Brown*, R Fern, JPL Jarvinen, K Kaila, BR Ransom

*Corresponding author for this work

Research output: Contribution to journalArticleScientificpeer-review

Abstract

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.

Original languageEnglish
Pages (from-to)1997-2000
Number of pages4
JournalNeuroreport
Volume9
Issue number9
Publication statusPublished - 22 Jun 1998
MoE publication typeA1 Journal article-refereed

Keywords

  • anoxia
  • axon
  • Ca2+
  • ion-sensitive microelectrodes
  • rat optic nerve
  • white matter
  • EXTRACELLULAR CALCIUM ACTIVITY
  • SPINAL-CORD
  • NA+-CA2+ EXCHANGER
  • INJURY
  • MECHANISMS
  • POTASSIUM
  • CONTUSION
  • CHANNELS

Cite this