《中国康复理论与实践》

《中国康复理论与实践》

• 基础研究 • 上一篇    下一篇

褪黑素对脊髓损伤大鼠突触可塑性的作用①

荆瀛黎1,2,3,4，刘小野5，白帆1,2,3,4，董浩1,2,3,4，陈惠1,2,3,4   

  1. 1. 首都医科大学康复医学院，北京市100068；2. 中国康复研究中心中国康复科学所，北京市100068；3. 北京脑重大疾病研究院神经损伤与修复研究所，北京市100068；4. 神经损伤与康复北京市重点实验室，北京市100068；5. 首都医科大学附属北京友谊医院，北京市100050。
  • 出版日期:2016-07-25 发布日期:2016-09-22

Effects of Melatonin on Synaptic Plasticity after Spinal Cord Injury in Rats

JING Ying-li1,2,3,4, LIU Xiao-ye5, BAI Fan1,2,3,4, DONG Hao1,2,3,4, CHEN Hui1,2,3,4   

  1. 1. Capital Medical University School of Rehabilitation Medicine, Beijing 100068, China; 2. Institute of Rehabilitation Science of China, China Rehabilitation Research Center, Beijing 100068, China; 3. Center of Neural Injury and Repair, Beijing Institute for Brain Disorders, Beijing 100068, China; 4. Beijing Municipal Key Laboratory for Neural Injury and Rehabilitation, Beijing 100068, China; 5. Beijing Friendship Hospital, Capital Medical University, Beijing 100050, China
  • Published:2016-07-25 Online:2016-09-22

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摘要： 目的探讨褪黑素对脊髓损伤后突触可塑性的影响。方法雌性Sprague-Dawley大鼠54 只分为假手术组(n=18)、对照组(n=18)和褪黑素组(n=18)。采用改良Allen 法复制大鼠T10中度损伤模型(10 g×25 mm)。免疫荧光法检测运动神经元数目，尼氏染色检测神经元中尼氏小体表达；Western blotting 检测神经纤维丝-200 (NF-200)、脑源性神经营养因子(BDNF)、突触素Ⅰ和神经生长相关蛋白-43 (GAP-43)的表达。结果术后7 d，与假手术组相比，对照组、褪黑素组运动神经元数、神经元中尼氏小体、NF-200、BDNF、突触素Ⅰ和GAP-43 表达下降；与对照组相比，褪黑素组运动神经元数、神经元中尼氏小体、NF-200、BDNF、突触素Ⅰ和GAP-43 的表达明显增加(P<0.01)。结论褪黑素能够修复损伤的突触可塑性，可能是促进运动功能恢复的机制。

关键词: 脊髓损伤, 突触可塑性, 褪黑素, 大鼠

Abstract: Objective To observe the effects of melatonin on synaptic plasticity impaired by spinal cord injury in rats. Methods A total of 54 female Sprague-Dawley rats were divided into sham group (n=18), control group (n=18) and melatonin group (n=18). Spinal cord injury model was established with modified Allen's method at T10 (10 g from 25 mm height). The number of neurons and the expression of the Nissl body were detected with immunofluorescence and Nissl staining. The expression of neurofilament-200 (NF-200), brain-derived neurotrophic factors (BDNF), Synapsin I and growth-associated protein-43 (GAP-43) was detected with Western blotting. Results Seven days after injury, the number of motoneurons, the expression of Nissl body in motoneurons, and the expression of BDNF, Synapsin I and GAP-43 decreased in the control group compared with those in the sham group, and they increased in the melatonin group compared with those in the control group. Conclusion Melatonin can repair the impaired synaptic plasticity, which might promote the functional recovery after spinal cord injury.

Key words: spinal cord injury, synaptic plasticity, melatonin, rats