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2010年02月04日

How Schwann cells assemble nodes of Ranvier

日 時 2010年02月04日(木) 13:00 より 14:00 まで
講演者 Elior Peles. Ph.D.
講演者所属 Hanna Hertz Professorial Chair for Multiple Sclerosis and Neuroscience, Department of Molecular Cell Biology,The Weizmann Institute of Science
お問い合わせ先 分子神経生理研究部門 池中一裕(内線:5249)
要旨

Saltatory conduction requires high-density accumulation of Na+ channels at nodes of Ranvier. Nodal Na+ channel clustering in the peripheral nervous system is regulated by myelinating Schwann cells through unknown mechanisms. We have recently found that channel clustering at heminodes bordering each myelin segment requires gliomedin, NrCAM and neurofascin 186, three cell adhesion molecules that mediate the interaction between Schwann cells and the axon. Furthermore, in the absence of heminodal clustering, Na+ channels still accumulate in mature nodes, a process that depends on axoglial contact at the adjacent paranodal junctions. Genetic removal of both nodal and paranodal axoglial contacts abolishes Na+ channel accumulation. Thus, Schwann cells serve a dual role in the assembly of the nodes of Ranvier by capturing Na+ channels at the edges of the forming myelin unit and by constraining their distribution between two myelin segments. Together, these two cooperating mechanisms ensure fast conduction in myelinated nerves.