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2-Vessel Occlusion/Hypotension: A Rat Model of Global Brain Ischemia
Published on: June 22, 2013
Changes in [Ca2+]0 during anoxia in CNS white matter
A M Brown1, R Fern, J P Jarvinen
1Department of Neurology, University of Washington School of Medicine, Seattle 98195, USA.
Neuroreport
|July 23, 1998
Summary
Anoxia causes irreversible axonal injury in rat optic nerves, requiring calcium (Ca2+). During prolonged anoxia, Ca2+ enters intracellular compartments, leading to nerve damage. Removing extracellular Ca2+ protects against this injury.
Area of Science:
- Neuroscience
- Cellular Biology
Background:
- Axonal injury during anoxia is Ca2+-dependent.
- The precise role of Ca2+ influx into intracellular compartments during anoxic injury is not fully understood.
Purpose of the Study:
- To investigate whether Ca2+ enters intracellular compartments during anoxia in the rat optic nerve.
- To determine the role of extracellular Ca2+ in anoxic axonal injury and functional recovery.
Main Methods:
- Monitoring extracellular Ca2+ concentration ([Ca2+]0) using ion-sensitive microelectrodes in rat optic nerve.
- Inducing periods of anoxia (15 min and 60 min) and reoxygenation.
- Manipulating extracellular Ca2+ levels in the bathing solution.
Main Results:
- Short anoxia (15 min) caused a transient, reversible increase in [Ca2+]0 due to extracellular space shrinkage, with temporary nerve conduction loss.
- Prolonged anoxia (60 min) led to an initial rise then a sustained fall in [Ca2+]0, indicating net Ca2+ influx into intracellular compartments.
- Ca2+ influx correlated with irreversible loss of nerve conduction after reoxygenation.
- Removal of extracellular Ca2+ prevented the anoxia-induced fall in [Ca2+]0 and protected against irreversible compound action potential loss.
Conclusions:
- Prolonged anoxia induces Ca2+ influx into intracellular compartments within the rat optic nerve.
- Extracellular Ca2+ is crucial for anoxic axonal injury and irreversible functional loss.
- Removing extracellular Ca2+ offers neuroprotection against anoxic damage to the optic nerve.
