How the axon, the most distal part of which may be placed over a metre away from the
neuronal cell body, receives metabolic substrates to generate ATP by residing mitochondria
is a fascinating aspect of fundamental neuroscience. The possibility that oligodendrocytes
and Schwann cells support axons independent of myelin was raised by the observation
of axon pathology without substantial demyelination or significant inflammatory response
in mice with dysfunctional oligodendrocytes, due to disruption of Plp1 and Cnp1 genes (
Nave and Trapp, 2008
). A number of groups have begun to unravel the metabolic aspects of axon–glial interaction
in both the central nervous system (CNS) and the peripheral nervous system (PNS).
These in vivo and in vitro studies were performed by disrupting mitochondrial respiratory chain in oligodendrocytes
and Schwann cells as well as by exploring lactate, an important metabolic substrate
for neurons, and its transport in the CNS.To read this article in full you will need to make a payment
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Article info
Publication history
Published online: August 06, 2013
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© 2013 Elsevier B.V. Published by Elsevier Inc. All rights reserved.
