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。
荆瀛黎1
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刘小野5
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白帆1
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董浩1
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陈惠1
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. 褪黑素对脊髓损伤大鼠突触可塑性的作用①[J]. 中国康复理论与实践, 2016
, 22(7)
: 774
-778
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DOI: 10.3969/j.issn.1006-9771.2016.07.007
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.
