Went fishing, cauqht a snake

A highly ordered, insulating layer of lipids and proteins known as the myelin sheath surrounds neuronal axons in our nervous system, allowing the rapid conduction of electrical impulses along nerve fibers. Myelin is laid down and maintained by dedicated neuroglia cells—oligodendrocytes in the central nervous system and Schwann cells in the peripheral nervous system. Formation of the myelin sheath is under strict axonal control and involves the wrapping of vast amounts of glial membrane around axons (1). The process is initiated by axon-glial cell contact, which elicits an adenosine 3′,5′-monophosphate (cAMP) signal within the glial cell. This signal drives myelin formation (2), but the molecular nature of the communication that triggers it has not been clear. On page 1402 of this issue, Monk et al. (3) provide compelling evidence for a cell surface receptor in Schwann cells that induces cAMP and myelin production in response to the targeted axon. An increase in the intracellular concentration of cAMP can partially restore the expression of myelin proteins in cultured mammalian Schwann cells, suggesting that cAMP is part of the signaling pathway that drives myelin formation in vivo. Inhibition of protein kinase A, the major target of cAMP, blocks myelination in cultured cells (4). Monk et al. report that gpr126, a heterotrimeric guanine nucleotide–binding protein (G protein)–coupled receptor, controls this signaling pathway.

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