The remarkable interaction between glial cells and axons is crucial for nervous system development and homeostasis. In the PNS, the intimate relationship between axons and Schwann cells culminates with the production of the myelin sheath, a multilamellar structure that is essential to insulate axons and ensure efficient propagation of the electric impulse. Further, glial cells regulate the organization of the axons, namely the formation of Nodes of Ranvier, and participate in their normal development and long-term survival. Neurons, in turn, promote proliferation, survival and differentiation of myelinating glia – most dramatically the formation of the myelin sheath. Several studies have shown that in the absence of glial cells neurons die, demonstrating that the survival of these two cell types in developing nerves is strictly linked. Accordingly, the morbidity associated to disorders of the nervou s system affecting myelin formation and/or stability can lead to neuronal cell death.
While the function of the myelin sheath in facilitating efficient and rapid propagation of action potentials by saltatory conduction has long been known, the molecular mechanisms responsible for its formation have remained elusive. In recent years our understanding of the proteins and of the molecular pathways required to initiate PNS myelination has significantly increased, however much less is known on the molecules required for the maintenance of the myelin sheath.
The nature of the signals and of the signaling pathways they control promoting myelin formation and maintenance, is the subject of this presentation. In our laboratory, we are interested in identifying the molecular mechanisms regulating how the cross talk between glial cells and axons is achieved during development and how it is impaired in pathological settings. The characterization of these signaling events is urgent and has clear translational application, as axonal suffering and neuronal cell death, are the main cause of morbidity in patients with progressed demyelinating disorders.
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