Expression of protein zero is increased in lesioned axon pathways in the central nervous system of adult zebrafish
Article first published online: 8 JAN 2003
Copyright © 2003 Wiley-Liss, Inc.
Volume 41, Issue 3, pages 301–317, February 2003
How to Cite
Schweitzer, J., Becker, T., Becker, C. G. and Schachner, M. (2003), Expression of protein zero is increased in lesioned axon pathways in the central nervous system of adult zebrafish. Glia, 41: 301–317. doi: 10.1002/glia.10192
- Issue published online: 8 JAN 2003
- Article first published online: 8 JAN 2003
- Manuscript Accepted: 1 NOV 2002
- Manuscript Received: 7 AUG 2002
- Deutsche Forschungsgemeinschaft. Grant Number: Be 1650/3-1
- Gemeinnützige Hertie-Stiftung
- Danio rerio;
- epithelial V-like antigen
The immunoglobulin superfamily molecule protein zero (P0) is important for myelin formation and may also play a role in adult axon regeneration, since it promotes neurite outgrowth in vitro. Moreover, it is expressed in the regenerating central nervous system (CNS) of fish, but not in the nonregenerating CNS of mammals. We identified a P0 homolog in zebrafish. Cell type-specific expression of P0 begins in the ventromedial hindbrain and the optic chiasm at 3–5 days of development. Later (at 4 weeks) expression has spread throughout the optic system and spinal cord. This is consistent with a role for P0 in CNS myelination during development. In the adult CNS, glial cells constitutively express P0 mRNA. After an optic nerve crush, expression is increased within 2 days in the entire optic pathway. Expression peaks at 1 to 2 months and remains elevated for at least 6 months postlesion. After enucleation, P0 mRNA expression is also upregulated but fails to reach the high levels observed in crush-lesioned animals at 4 weeks postlesion. Spinal cord transection leads to increased expression of P0 mRNA in the spinal cord caudal to the lesion site. The glial upregulation of P0 mRNA expression after a lesion of the adult zebrafish CNS suggests roles for P0 in promoting axon regeneration and remyelination after injury. GLIA 41:301–317, 2003. © 2003 Wiley-Liss, Inc.