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Axon function persists during anoxia in mammalian white matter
Selva Baltan Tekkök1, Angus M Brown, Bruce R Ransom
1Department of Neurology, University of Washington School of Medicine, Seattle, Washington, USA. selva@u.washington.edu
Summary
White matter axons show surprising anaerobic energy capacity, especially with sufficient glucose. This challenges previous assumptions about central nervous system anoxia resistance.
Area of Science:
- Neuroscience
- Cellular Metabolism
- Physiology
Background:
- Central nervous system (CNS) axons typically fail rapidly during anoxia, suggesting limited anaerobic capacity.
- Previous studies implied a lack of anaerobic energy reserves in CNS white matter.
Purpose of the Study:
- To reassess the anaerobic capacity of rodent white matter axons.
- To investigate the role of glucose availability in anoxic axon survival.
Main Methods:
- Used mouse and rat optic nerves to study axon function under anoxic and cyanide conditions.
- Measured axon function semiquantitatively via the area under the compound action potential.
- Manipulated glucose concentration in artificial cerebrospinal fluid (CSF).
Main Results:
- Mouse optic nerves maintained significant function during anoxia/cyanide, dependent on glucose.
- Rat optic nerves showed rapid function loss under anoxia, but improved with higher glucose concentrations (30 mmol/L).
- Anoxia duration correlated with reduced compound action potential area in mouse optic nerves (up to 70% loss after 90 min).
Conclusions:
- White matter exhibits resistance to anoxia, with some axons utilizing anaerobic energy.
- Glucose availability and diffusion are critical for white matter axon survival during anoxia.
- Findings impact understanding of white matter energy metabolism and ischemic injury susceptibility.