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The Journal of Neuroscience, October 22, 2008, 28(43):11003-11014; doi:10.1523/JNEUROSCI.3285-08.2008

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Cellular/Molecular
Maintenance of Axo-Oligodendroglial Paranodal Junctions Requires DCC and Netrin-1

Andrew A. Jarjour,^1,2 Sarah-Jane Bull,^1,2 Mohammadali Almasieh,⁴ Sathyanath Rajasekharan,^1,2 K. Adam Baker,^1,2 Jeannie Mui,³ Jack P. Antel,^1,2 Adriana Di Polo,⁴ and Timothy E. Kennedy^1,2,3

¹Montreal Neurological Institute, Departments of ²Neurology and Neurosurgery and ³Anatomy and Cell Biology, McGill University, Montreal, Quebec, Canada H3A 2B4, and ⁴Department of Pathology and Cell Biology, Université de Montréal, Montreal, Quebec, Canada H3T 1J4

Correspondence should be addressed to Timothy E. Kennedy, Centre for Neuronal Survival, Montreal Neurological Institute, McGill University, 3801 University Avenue, Montreal, Quebec, Canada H3A 2B4. Email: timothy.kennedy{at}mcgill.ca

Paranodal axoglial junctions are essential for the segregation of myelinated axons into distinct domains and efficient conduction of action potentials. Here, we show that netrin-1 and deleted in colorectal cancer (DCC) are enriched at the paranode in CNS myelin. We then address whether netrin-1 signaling influences paranodal adhesion between oligodendrocytes and axons. In the absence of netrin-1 or DCC function, oligodendroglial paranodes initially develop and mature normally but later become disorganized. Lack of DCC or netrin-1 resulted in detachment of paranodal loops from the axonal surface and the disappearance of transverse bands. Furthermore, the domain organization of myelin is compromised in the absence of netrin-1 signaling: K⁺ channels inappropriately invade the paranodal region, and the normally restricted paranodal distribution of Caspr expands longitudinally along the axon. Our findings identify an essential role for netrin-1 and DCC regulating the maintenance of axoglial junctions.

Key words: myelin; axoglial junction; paranode; septate-like junctions; Caspr; neurofascin

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Received July 14, 2008; revised Aug. 26, 2008; accepted Sept. 8, 2008.

Correspondence should be addressed to Timothy E. Kennedy, Centre for Neuronal Survival, Montreal Neurological Institute, McGill University, 3801 University Avenue, Montreal, Quebec, Canada H3A 2B4. Email: timothy.kennedy{at}mcgill.ca

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