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Oligodendrocytes regulate formation of nodes of Ranvier via the recognition molecule OMgp

  • DU-YU NIE (a1) (a2), QUAN-HONG MA (a1) (a3), JANICE W.S. LAW (a4), CHERN-PANG CHIA (a4), NARENDER K. DHINGRA (a4), YASUSHI SHIMODA (a5), WU-LIN YANG (a4), NENG GONG (a6), QING-WEN CHEN (a4) (a7), GANG XU (a4), QI-DONG HU (a1) (a2), PIERCE K.H. CHOW (a8), YEE-KONG NG (a2), ENG-ANG LING (a2), KAZUTADA WATANABE (a5), TIAN-LE XU (a6), AMYN A. HABIB (a9), MELITTA SCHACHNER (a3) (a10) and ZHI-CHENG XIAO (a1) (a2) (a4)...

The molecular mechanisms underlying the involvement of oligodendrocytes in formation of the nodes of Ranvier (NORs) remain poorly understood. Here we show that oligodendrocyte-myelin glycoprotein (OMgp) aggregates specifically at NORs. Nodal location of OMgp does not occur along demyelinated axons of either Shiverer or proteolipid protein (PLP) transgenic mice. Over-expression of OMgp in OLN-93 cells facilitates process outgrowth. In transgenic mice in which expression of OMgp is down-regulated, myelin thickness declines, and lateral oligodendrocyte loops at the node-paranode junction are less compacted and even join together with the opposite loops, which leads to shortened nodal gaps. Notably, each of these structural abnormalities plus modest down-regulation of expression of Na+ channel α subunit result in reduced conduction velocity in the spinal cords of the mutant mice. Thus, OMgp that is derived from glia has distinct roles in regulating nodal formation and function during CNS myelination.

Corresponding author
Neurobiology Lab, Department of Clinical Research, Singapore General Hospital, Block A, No. 7 Hospital Drive, Singapore 169608, phone: +65 6326 6195, fax: +65 6321 3606, email:
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Neuron Glia Biology
  • ISSN: 1740-925X
  • EISSN: 1741-0533
  • URL: /core/journals/neuron-glia-biology
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