Figure 2. Oligodendrocytes provide metabolic support to neurons.

(A) Normal myelin with compacted (dark blue) and uncompacted (light blue) channels form a multilamellar structure around the axon. (B) In PLP-null animals, myelin appears to be ultrastructurally normal, but the underlying axons show signs of degeneration. (C) In MBP-null mice (shiverer mice), only a thin sheath of uncompacted myelin wraps the axon. Despite this dysmyelination, these mice develop normally and axons are intact. (D) The myelin in CNPase-null mice is more compacted than normal as a result of the loss of the uncompacted myelinic channels, resulting in severe axonal degeneration. (E) Loss of MCT1 in oligodendrocytes leads to axonal degeneration despite normal-appearing myelin wrapping the axons. All these models show a clear distinction between the ability of myelin to support axonal conductance and its ability to provide trophic support to the axon. How myelinic channels are affected in the PLP- and MCT1-null mice remains to be elucidated.