脑源性神经营养因子mRNA在胚胎脊髓修复成鼠脊髓损伤过程中的变化

Changes of BDNF mRNA by molecular hybridization during embryonic spinal cord repairing injury of adult rats

观察脑源性神经营养因子（ＢＤＮＦ）在胚胎脊髓修复成鼠损伤脊髓过程中的变化。方法将妊娠１４天胚胎脊髓植入急性损伤的成体脊髓后１、３、５、７、１０、１５和３０天，用原位和斑点分子杂交技术对胚胎脊髓和正常脊髓内ＢＤＮＦｍＲＮＡ的表达变化作了定性和定量观察。结果在正常脊髓内，ＢＤＮＦｍＲＮＡ以前角运动神经元和少量胶质细胞分布为主；脊髓损伤后，杂交产物扩大到中小型神经元，同时更多的胶质细胞参与了反应；胚胎脊髓移植后，除移植物本身继续维持表达外，正常脊髓阳性反应神经元和胶质细胞数量进一步增加。损伤组原位和斑点分子杂交的反应强度明显高于正常组，而移植组的分子杂交反应又在很多时相点上显著高于损伤组。结论移植的胚胎脊髓除为自身和宿主脊髓提供神经营养外，也诱发了正常脊髓在发生过程中曾经拥有的合成机制，以增强神经营养因子表达的方式为自身的再生提供营养，同时也为移植物的发育分化提供合适的营养环境。

Objective To study the changes of (brain derived neurotrophic factor) BDNF mRNA during embroyonic spinal cord repairing spinal cord injury of adult rats. Methods At day 1,3,5,7,10,15, and 30 after embryonic spinal cord being transplanted into acutely injured spinal cord of adult rats, changes of BDNF mRNA within donor tissue and host tissue were demonstrated qualitatively and quantitatively by in situ hybridization and dot hybridization. Results Qualitatively, BDNF mRNA was mainly expressed within cytoplasm of motor neurons and a few gliocytes in normal spinal cord. After spinal cord injury, hybridizing products expanded to the mediate and small sized neurons, also more gliocytes took part in hybridization response. Following transplantation, positively hybridizing neurons and gliocytes increased in number in host tissue, and embryonic spinal cord kept an expressing level similar to that before being transplanted. It was also revealed quantitatively that reacting intensity of the cells in the injured group was strikingly higher than that in the normal group. However, hybridization intensity in the transplanted group was even higher at many intervals than that in the injured group. Besides, the lasting period for hybridization reaction in the transplanted group was also different from that in the injured group. The most intensive reacting phase in the former presented at day 10 and 15, and in the latter at day 7 after operation. Conclusions We suggest that transplanted embryonic spinal cord can, besides provision neurol trophines for itself and host spinal cord, evoke synthetic mechanisms of host spinal cord once holding during its embryonic development so as to enhance expression of the neurotrophin. In this way, the host spinal cord may provide neurotrophin for its regeneration and provide an trophic environment for the grafts to develop and differentiate.