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The Journal of Neuroscience, July 28, 2004, 24(30):6826-6832; doi:10.1523/JNEUROSCI.1856-04.2004

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Cellular/Molecular
Promotion of Axon Regeneration by Myelin-Associated Glycoprotein and Nogo through Divergent Signals Downstream of G_i/G

Yuiko Hasegawa,^1,2 * Masashi Fujitani,^1 * Katsuhiko Hata,¹ Masaya Tohyama,² Satoru Yamagishi,¹ and Toshihide Yamashita¹

¹Department of Neurobiology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan, and ²Department of Anatomy and Neuroscience, Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan

Several myelin-derived proteins have been identified as components of the CNS myelin that prevents axonal regeneration in the adult vertebrate CNS. Activation of RhoA has been shown to be an essential part of the signaling mechanism of these proteins. Here we report an additional signal, which determines whether these proteins promote or inhibit axon outgrowth. Myelin-associated glycoprotein (MAG) and Nogo trigger the intracellular elevation of Ca²⁺ as well as the activation of PKC, presumably mediated by G_i/G. Neurite outgrowth inhibition and growth cone collapse by MAG or Nogo can be converted to neurite extension and growth cone spreading by inhibiting conventional PKC, but not by inhibiting inositol 1,4,5-triphosphate (IP₃). Conversely, neurite growth of immature neurons promoted by MAG is abolished by inhibiting IP₃. Activation of RhoA is independent of PKC. Thus, a balance between PKC and IP₃ is important for bidirectional regulation of axon regeneration by the myelin-derived proteins.

Key words: p75; myelin; myelin-derived proteins; G-protein; PKC; spinal

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Received April 6, 2004; revised June 10, 2004; accepted June 11, 2004.

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