Abstract
Objective
To explore the relationship between cerebrospinal fluid-contacting neurons (CSF-cNs) and endogenous neural progenitor cells (ENPCs) and whether CSF-cNs are involved in nerve repair after spinal cord injury (SCI).
Methods
Cholera toxin B-horseradish peroxidase complex (CB-HRP) and cholera toxin B conjugated with saporin (CB-SAP) were injected into the lateral ventricles of spinal cord injured rats to mark and destroy the CSF-cNs. Then the rats in the experimental group were injured by SCI. Observe the content and co-expression of CSF-cNs and ENPCs in rats of each group, and observe the recovery of motor function after SCI in each group.
Results
After the destruction of CSF-cNs, the number of ENPCs decreased significantly in the long term after the surgery, and the recovery of motor function also deteriorated as compared to the group with intact CSF-cNs. Meanwhile some cells in the spinal cord express both the biological marker of CSF-cNs and ENPCs.
Conclusion
This study shows that the population of ENPCs and motor function recovery in SCI rats declined after the destruction of CSF-cNs, suggesting that CSF-cNs affect the ENPCs population and may be involved in the recovery of neural function after SCI.
Author contributions
Qing Li and Lei-luo Yang designed the study. Li Chen, Wen-bo Zhao, and Jing Shan participated in SCI modeling and immunofluorescence. Yu-qi He, Xue-xing Shi and Zong-long Lin participated in SCI modeling, BBB data analysis, and Slant board movement score analysis. Yu-qi He and Xue-xing Shi wrote the manuscript. Qing Li and Lei-luo Yang revised the manuscript. All authors have read and approved final version of the manuscript.
Acknowledgements
We would like to thank Xiao-wei Dou (Guizhou Medical University) for technical support for the present study. We would also like to thank all the laboratory members of Clinical Research Center of Affiliated Hospital of Guizhou Medical University for their encouragement and generous support for the present study.
Disclosure statement
No potential conflict of interest was reported by the author(s).