Sammendrag
Mitochondria play several crucial roles in the life of oligodendrocytes. During development of the myelin sheath they are essential
providers of carbon skeletons and energy for lipid synthesis. During normal brain function their consumption of pyruvate will
be a key determinant of how much lactate is available for oligodendrocytes to export to power axonal function. Finally, during
calcium-overload induced pathology, as occurs in ischemia, mitochondria may buffer calcium or induce apoptosis. Despite their
important functions, very little is known of the properties of oligodendrocyte mitochondria, and mitochondria have never been
observed in the myelin sheaths. We have now used targeted expression of fluorescent mitochondrial markers to characterize
the location and movement of mitochondria within oligodendrocytes. We show for the first time that mitochondria are able to
enter and move within the myelin sheath. Within the myelin sheath the highest number of mitochondria was in the cytoplasmic
ridges along the sheath. Mitochondria moved more slowly than in neurons and, in contrast to their behavior in neurons and
astrocytes, their movement was increased rather than inhibited by glutamate activating NMDA receptors. By electron microscopy
we show that myelin sheath mitochondria have a low surface area of cristae, which suggests a low ATP production. These
data specify fundamental properties of the oxidative phosphorylation system in oligodendrocytes, the glial cells that enhance
cognition by speeding action potential propagation and provide metabolic support to axons.
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