The Cell Neural Adhesion Molecule Contactin-2 (TAG-1) Is Beneficial for Functional Recovery after Spinal Cord Injury in Adult Zebrafish
- Authors
- Lin, J.F., Pan, H.C., Ma, L.P., Shen, Y.Q., and Schachner, M.
- ID
- ZDB-PUB-130110-14
- Date
- 2012
- Source
- PLoS One 7(12): e52376 (Journal)
- Registered Authors
- Schachner, Melitta
- Keywords
- none
- MeSH Terms
-
- Aging/metabolism*
- Animals
- Axons/metabolism
- Axons/pathology
- Contactin 2/genetics
- Contactin 2/metabolism*
- Gene Knockdown Techniques
- Locomotion
- Motor Neurons/metabolism
- Motor Neurons/pathology
- RNA, Messenger/genetics
- RNA, Messenger/metabolism
- Recovery of Function*
- Spinal Cord Injuries/metabolism*
- Spinal Cord Injuries/pathology
- Spinal Cord Injuries/physiopathology*
- Time Factors
- Up-Regulation/genetics
- Zebrafish/metabolism*
- Zebrafish Proteins/metabolism*
- PubMed
- 23285014 Full text @ PLoS One
The cell neural adhesion molecule contactin-2 plays a key role in axon extension and guidance, fasciculation, and myelination during development. We thus asked, whether contactin-2 is also important in nervous system regeneration after trauma. In this study, we used an adult zebrafish spinal cord transection model to test the functions of contactin-2 in spinal cord regeneration. The expression patterns of contactin-2 at different time points after spinal cord injury were studied at the mRNA level by qPCR and in situ hybridization, and contactin-2 protein levels and immunohistological localization were detected by Western blot and immunofluorescence analyses, respectively. Contactin-2 mRNA and protein levels were increased along the central canal at 6 days and 11 days after spinal cord injury, suggesting a requirement for contactin-2 in spinal cord regeneration. Co-localization of contactin-2 and islet-1 (a motoneuron marker) was observed in spinal cords before and after injury. To further explore the functions of contactin-2 in regeneration, an anti-sense morpholino was used to knock down the expression of contactin-2 protein by application at the time of injury. Motion analysis showed that inhibition of contactin-2 retarded the recovery of swimming functions when compared to standard control morpholino. Anterograde and retrograde tracing at 6 weeks after injury showed that knock down of contactin-2 inhibited axonal regrowth from NMLF neurons beyond lesion site. The combined observations indicate that contactin-2 contributes to locomotor recovery and successful regrowth of axons after spinal cord injury in adult zebrafish.