Xiangzhe Li1,2,3, Qinfeng Wu2,3, Caizhong Xie4, Can Wang5, Qinghua Wang6, Chuanming Dong7, Lu Fang1, Jie Ding1, Tong Wang8. 1. Rehabilitation Medicine Center, The First Affiliated Hospital of Nanjing Medical University, 210029, Nanjing, China. 2. Rehabilitation Medicine Center, Suzhou Science & Technology Town Hospital, 215153, Suzhou, Jiangsu, China. 3. Rehabilitation Medicine Center, Suzhou Hospital Affiliated to Nanjing Medical University, 215153, Suzhou, Jiangsu, China. 4. Department of Rehabilitation Medicine, Nanjing General Hospital, 210000, Nanjing, China. 5. Children's Development Center, Suzhou Municipal Hospital, 215008, Suzhou, Jiangsu, China. 6. Experimental Animal Center, Nantong University, 226021, Nantong, Jiangsu, China. 7. Department of Human Anatomy, Medical College of Nantong University, 226021, Nantong, Jiangsu, China. 8. Rehabilitation Medicine Center, The First Affiliated Hospital of Nanjing Medical University, 210029, Nanjing, China. wangtong60621@163.com.
Abstract
STUDY DESIGN: Experimental study. OBJECTIVES: To investigate the role of BDNF-TrkB signaling that promotes the recovery of neurological function in rats with incomplete spinal cord injury (SCI) after treadmill training (TT). SETTING: Rehabilitation Medicine Center of the First Affiliated Hospital of Nanjing Medical University, Nanjing, China. METHODS: Forty rats were divided into five groups: (i) Sham; (ii) SCI and phosphate-buffered saline (PBS) (SCI/PBS); (iii) SCI-TT/PBS; (iv) SCI/TrkB-IgG; and (v) SCI-TT/TrkB-IgG. The intrathecal catheter and T10 contusion SCI model was established. At 7-day post SCI, the BDNF-TrkB signaling was blocked by TrkB-IgG. Exercise began at 8th day after SCI and continued for 4 weeks. The BBB scale and motor-evoked potential (MEP) were used for the evaluation of the locomotor functions. The BDNF/TrkB, PSD-95, SYP synthesis, and neuroprotective effect was determined by western blot, Nissl, or immunohistochemistry staining. RESULTS: The expression of BDNF and TrkB in the SCI-TT/PBS group was 1.46 ± 0.09 and 1.70 ± 0.22, respectively, higher than that in SCI/PBS group (0.51 ± 0.04 and 0.76 ± 0.07, respectively), relative to the Sham group. The BBB scores in the Sham, SCI/PBS, SCI-TT/PBS, SCI/TrkB-IgG, and SCI-TT/TrkB-IgG groups were 21.00 ± 0.00, 7.63 ± 0.74, 12.13 ± 1.36, 7.88 ± 0.64, and 8.75 ± 0.88, respectively. The percentages of MEP responders/non-responders were 100, 0, 75, 0, and 50%. The MEP latencies in Sham, SCI-TT/PBS, and SCI-TT/TrkB-IgG groups were 6.65 ± 0.19, 13.32 ± 2.95, and 19.55 ± 4.55 ms, respectively. The number of NeuN+ neurons, the cell body area of motor neurons, PSD-95, and SYP expression in the SCI-TT/PBS group was significantly higher than that in the SCI/PBS, SCI/TrkB-IgG, and SCI-TT/TrkB-IgG groups. CONCLUSION: The BDNF-TrkB signaling is a critical pathway in exercise training that promotes the recovery of neurological function in rats with incomplete SCI.
STUDY DESIGN: Experimental study. OBJECTIVES: To investigate the role of BDNF-TrkB signaling that promotes the recovery of neurological function in rats with incomplete spinal cord injury (SCI) after treadmill training (TT). SETTING: Rehabilitation Medicine Center of the First Affiliated Hospital of Nanjing Medical University, Nanjing, China. METHODS: Forty rats were divided into five groups: (i) Sham; (ii) SCI and phosphate-buffered saline (PBS) (SCI/PBS); (iii) SCI-TT/PBS; (iv) SCI/TrkB-IgG; and (v) SCI-TT/TrkB-IgG. The intrathecal catheter and T10 contusion SCI model was established. At 7-day post SCI, the BDNF-TrkB signaling was blocked by TrkB-IgG. Exercise began at 8th day after SCI and continued for 4 weeks. The BBB scale and motor-evoked potential (MEP) were used for the evaluation of the locomotor functions. The BDNF/TrkB, PSD-95, SYP synthesis, and neuroprotective effect was determined by western blot, Nissl, or immunohistochemistry staining. RESULTS: The expression of BDNF and TrkB in the SCI-TT/PBS group was 1.46 ± 0.09 and 1.70 ± 0.22, respectively, higher than that in SCI/PBS group (0.51 ± 0.04 and 0.76 ± 0.07, respectively), relative to the Sham group. The BBB scores in the Sham, SCI/PBS, SCI-TT/PBS, SCI/TrkB-IgG, and SCI-TT/TrkB-IgG groups were 21.00 ± 0.00, 7.63 ± 0.74, 12.13 ± 1.36, 7.88 ± 0.64, and 8.75 ± 0.88, respectively. The percentages of MEP responders/non-responders were 100, 0, 75, 0, and 50%. The MEP latencies in Sham, SCI-TT/PBS, and SCI-TT/TrkB-IgG groups were 6.65 ± 0.19, 13.32 ± 2.95, and 19.55 ± 4.55 ms, respectively. The number of NeuN+ neurons, the cell body area of motor neurons, PSD-95, and SYP expression in the SCI-TT/PBS group was significantly higher than that in the SCI/PBS, SCI/TrkB-IgG, and SCI-TT/TrkB-IgG groups. CONCLUSION: The BDNF-TrkB signaling is a critical pathway in exercise training that promotes the recovery of neurological function in rats with incomplete SCI.
Authors: Johnny D Figueroa; Kathia Cordero; Keisha Baldeosingh; Aranza I Torrado; Robert L Walker; Jorge D Miranda; Marino De Leon Journal: J Neurotrauma Date: 2011-11-07 Impact factor: 5.269
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