Yu-Qi He1,2, Xue-Xing Shi3, Li Chen4, Wen-Bo Zhao5, Jing Shan6, Zong-Long Lin1,2, Lei-Luo Yang2, Qing Li2. 1. School of Clinical Medicine, Guizhou Medical University, Guiyang, P.R. China. 2. Department of Traumatic Orthopedics, Affiliated Hospital, Guizhou Medical University, Guiyang, P.R. China. 3. Department of Orthopedics, Affiliated Baiyun Hospital, Guizhou Medical University, Guiyang, P.R. China. 4. Department of Orthopedics, Dazhou Central Hospital, Dazhou, P.R. China. 5. Department of first Orthopedics, Fifth Affiliated (zhuhai) Hospital, Zunyi Medical University, Zhuhai, P.R. China. 6. Department of Orthopedics, First Affiliated Hospital, Nanchang University, Nanchang, P.R. China.
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.
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.