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The Journal of Neuroscience, October 1, 2001, 21(19):7568-7575

Localization of Caspr2 in Myelinated Nerves Depends on Axon-Glia Interactions and the Generation of Barriers along the Axon

Sebastian Poliak¹, Leora Gollan¹, Daniela Salomon¹, Erik O. Berglund², Reiko Ohara³, Barbara Ranscht², and Elior Peles¹

¹ Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot 76100, Israel, ² The Burnham Institute, Neurobiology Program, La Jolla, California 92037, and ³ Department of Human Gene Research at Kazusa DNA Research Institute, Chiba 292-0812, Japan

Cell recognition proteins of the contactin-associated protein (Caspr) family demarcate distinct domains along myelinated axons. Caspr is present at the paranodal junction formed between the axon and myelinating glial cells, whereas Caspr2 is localized and associates with K⁺ channels at the adjacent juxtaparanodal region. Here we investigated the distribution of Caspr2 during development of peripheral nerves of normal and galactolipids-deficient [ceramide galactosyl transferase (CGT)/] mice. This mutant exhibits paranodal abnormalities, lacking all putative adhesion components of this junction, including Caspr, contactin, and neurofascin 155. In sciatic nerves of this mutant, Caspr2 was not found at the juxtaparanodal region but was concentrated instead at the paranodes with Kv1.2. Similar distribution of Caspr2 was found in the PNS of contactin knock-out mice, which also lack Caspr in their paranodes. During development of wild-type peripheral nerves, Caspr2 and Kv1.2 were initially detected at the paranodes before relocating to the adjacent juxtaparanodal region. This transition was not observed in CGT mice, where Caspr2 and Kv1.2 remained paranodal. Double labeling for Caspr and Caspr2 demonstrated that these two related proteins occupied mutually excluding domains along the axon and revealed the presence of both paranodal and internodal barrier-like structures that are delineated by Caspr. Finally, we found that the disruption of axon-glia contact in CGT/ nerves also affects the localization of the cytoskeleton-associated protein 4.1B along the axon. Altogether, our results reveal a sequential appearance of members of the Caspr family at different domains along myelinated axons and suggest that the localization of Caspr2 may be controlled by the generation of Caspr-containing barriers along the axon.

Key words: Caspr2; myelin; node of Ranvier; axo-glial junction; Schwann cells; K⁺ channels

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Copyright © 2001 Society for Neuroscience  0270-6474/01/21197568-08$05.00/0

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