AXONAL SIGNALS AND MYELINOGENESIS IN THE CENTRAL-NERVOUS-SYSTEM

Citation
C. Lubetzki et al., AXONAL SIGNALS AND MYELINOGENESIS IN THE CENTRAL-NERVOUS-SYSTEM, MS. Medecine sciences, 13(10), 1997, pp. 1097-1105
Citations number
36
Categorie Soggetti
Medicine, Research & Experimental
Journal title
ISSN journal
07670974
Volume
13
Issue
10
Year of publication
1997
Pages
1097 - 1105
Database
ISI
SICI code
0767-0974(1997)13:10<1097:ASAMIT>2.0.ZU;2-B
Abstract
Oligodendrocytes, in the central nervous system (CNS), and Schwann cel ls, in the peripheral nervous system (PNS), have the unique ability to synthesize large amounts of membrane that wrap around axons and compa ct to form myelin. The close interaction between axons and myelin form ing,cells, suggests the existence of mutual cross-talks between the ne urons and their myelinating partners. Indeed, in the peripheral nervou s system it is now well established that axonal signals are mandatory at all the stages of Schwann cell precursors development into myelin-f orming cells and that the signal for nerve engulfment and ensheathment originates in axons with which mature Schwann cells interact. Until r ecently, it was generally assumed that, in contrast to Schwann cells, oligodendrocytes developped independently from neurons. Here we review results from several laboratories suggesting that neurons influence m yelinogenesis. Early during embryonic development neurons may play a r ole in the induction of oligodendrocytes precursors. Later on, prolife ration and survival of oligodendrocytes progenitors have been shown to depend on electrical activity in axons. At the time of myelination, t he existence of a specific axonal signal allowing oligodendrocyte proc esses to recognize axons from dendrites, has been put forward and the induction of the myelination process seems to depend on neuronal elect rical activity. Finally, neurons may influence the rate of myelin prot ein synthesis and normal myelin compaction requires axonal signaling. The implications of these recent findings are discussed in the perspec tive of the physiopathology of demyelinating disease and of emerging t herapeutical strategies aimed at myelin repair.