神经营养因子3在电刺激治疗脊髓损伤中的作用

The function of NT-3 in electrical treatment for spinal cord injury

目的 探讨神经营养因子-3（NT-3）在成年猫脊髓损伤后电刺激治疗中的作用.方法 成年猫25只,雌雄不拘,随机分为左侧脊神经根去传入手术组（手术组,保留L6脊神经节）、手术＋电刺激组（电刺激组）、手术＋电刺激＋NT-3抗体封闭组（抗体封闭组）,2个月后对相应脊髓节段和保留脊神经节进行霍乱毒素B亚单位结合辣根过氧化物酶复合物形态学示踪及免疫组化、酶组化染色观察并进行组间比较.结果 各组脊神经节感觉性神经元中枢投射轴突终末集中分布在脊髓后角Ⅲ、Ⅳ、Ⅴ板层内侧,但电刺激组终末出芽标记点密度高于手术组,而抗体封闭组终末再生出芽能力相比电刺激组显著降低.结论 电刺激可能通过上调NT-3的表达促进损伤脊髓和感觉神经元的形态和功能修复,来参与脊髓可塑性过程.

Objective To investigate the effect of endogenous neurotrophin-3 （NT-3） in treatment of spine cord injury with electro-acupuncture （EA） . Methods Twenty five adult cats were divided into 3 groups： spine injury group, injury＋electric acupuncture （EA） group and injury＋EA＋NT-3 antibody block group. The left 1st to 5th lumbar （L1-L5）, and the 7th lumbar （L7） to the 2nd sacral （S2） dorsal root ganglion （DRG） were exposed and removed at their respective intervertebral foramina, leaving the L6 DRG intact. Two months later, the spinal cord segments and the spared DRG were examined by CB-HRP transganglionic tracing, histochemistry and enzymohistochemistry analysis, respectively. Results NT-3 positive immune reaction was mainly dis- tributed in large-sized neurons in DRG. In contrast, in spinal dorsal horn, NT-3-1R was mainly distributed in part of neurons in lamina II. After EA, the number of positive large-sized neurons for NT-3 in DRG and in lamina II increased than those in opera- tion group （P〈0.05）. CB-HRP tracing showed that the regeneration sprouting of large sensory neuron of DRG were major dis- tributed in the III, IV, V layers of spinal dorsal horn; the densities of terminal sprouting derived from spared DRG were greaterly in- creased in EA group than that in the non-EA group （P〈0.05）. However, after using NT-3 antibody, the densities of terminal sprouting derived from spared DRG decreased markedly compared to that of EA group （P〈0.05）. Conclusion The regeneration sprouting of large sensory neuron of DRG at the later stage are mainly distributed in the deep layers （Ⅲ, Ⅳ, Ⅴ layers） of spinal dorsal horn. EA may enhance the spinal cord plasticity through up-regulating the expression of NT-3, which promote the repair of injured spinal cord and sensory neurons in DRG.