大鼠体神经-内脏神经吻合后脑源性神经营养因子及其受体的表达变化

EXPRESSION CHANGES OF BDNF AND ITS RECEPTOR AFTER SOMATIC-AUTONOMIC NERVE ANASTOMOSIS IN THE RAT

为了研究大鼠体神经-内脏神经吻合后脑源性神经营养因子(BDNF)及其受体酪氨酸激酶B(TrkB)在脊髓前角神经元中的表达变化,以正常大鼠为对照,运用RT-PCR技术检测大鼠体神经-内脏神经吻合术后不同时间脊髓腰4(L4)前角神经元中BDNF及TrkB mRNA的表达变化。结果显示,在正常大鼠L4前角神经元中,BDNF及TrkB的mRNA均存在一定水平的表达;体神经-内脏神经吻合术后7d、14d、1m和2m,BDNF和TrkBm RNA的表达均升高,术后7d达到高峰,14d开始下降;2m时BD-NF mRNA的表达量仍显著高于正常组(P<0.01),而TrkB mRNA的表达量到2m时虽仍高,但与正常组相比,其差异已无统计学意义(P>0.05)。上述结果表明,大鼠体神经-内脏神经反射弧建立后,脊髓L4前角神经元的内源性BDNF及其受体TrkB的表达均增高,它们可能作为保护性因子有利于受损神经元的存活和再生。

In order to study the expression changes of brain-derived neurotrophic factor （BDNF） and its receptor tyrosine kinase B （TrkB） in ventral horn neurons of spinal cord after somatic-autonomic ventral root （VR） anastomosis in the rat, reverse transeription-pelymerase chain reaction （RT-PCR） technique was applied to detect the expression changes of BDNF and TrkB mRNAs in the ventral horn neurons at the lumbar 4 segment （ L4 ） at different periods after the somatic-autonomic reflex pathway was established by intra-dural microanastomosis of the left L4 VR to L6 VR, while normal rats were used as control. The results revealed that there existed BDNF and TrkB mRNA expressions in normal L4 ventral horn neurons. BDNF and TrkB mRNA expressions were increased at the 7th day, 14th day, 1 month and 2 months, respectively, after L4-L6 VRs anastomosis. Their expressions reached peak at the 7th day and began to decrease at the 14th day. BDNF mRNA expression was still significantly higher than that in the control group on 2 months （ P 〈 0.01 ）. TrkB mRNA expression was increased a little on 2 months, but with no significant difference compared with the control group （ P 〉 0.05 ）. The present results indicate that BDNF and TrkB mRNA expressions have been increased in L4 ventral horn neurons of spinal cord after establishing the somatic-autonomic reflex arc. The endogenous increases of BDNF and TrkB might serve as protective factors which benefit the survival and regeneration of the injured motor neurons.