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Schwann cell glycogen selectively supports myelinated axon function
Angus M Brown1, Richard D Evans, Joel Black
1School of Biomedical Sciences, University of Nottingham, Nottingham, United Kingdom. ambrown@nottingham.ac.uk
Annals of Neurology
|October 5, 2012
Summary
Peripheral nerve glycogen supports large myelinated axon function during glucose deprivation by providing energy. Small unmyelinated axons, however, are not protected by glycogen and are more susceptible to damage from low glucose levels.
Area of Science:
- Neuroscience
- Cell Biology
- Biochemistry
Background:
- Axon loss can result from interrupted energy supply.
- Glycogen's role in peripheral nerve energy metabolism was previously unclear.
Purpose of the Study:
- To determine if glycogen is present in mammalian peripheral nerve.
- To investigate if glycogen supports axon conduction during aglycemia (glucose deprivation).
Main Methods:
- Biochemical assays and electron microscopy to detect glycogen.
- Electrophysiology to assess axon function (compound action potential - CAP).
Main Results:
- Glycogen was found in sciatic nerve, mainly in Schwann cells, and its levels correlated with ambient glucose.
- During aglycemia, large myelinated axon (A fiber) conduction failure paralleled glycogen depletion.
- Glycogen content predicted CAP failure latency in A fibers; glycogen did not benefit unmyelinated C fibers.
Conclusions:
- Peripheral nerve glycogen, primarily in Schwann cells, exclusively supports large myelinated axon conduction during aglycemia.
- Glycogen breakdown likely provides lactate to myelinated axons for energy.
- Unmyelinated axons lack glycogen protection and are vulnerable during hypoglycemia.
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