面神经切断及修复后面神经核内受体酪氨酸激酶B和C mRNA的变化

Changes of trkB and trkC mRNA in facial nucleus after axotomy and end-to-end anastomsis in the rat

目的 探讨面神经损伤及修复条件下面神经核运动神经元受体酪氨酸激酶B和C(receptortyrossinekinaseB C ,trkB和trkC )mRNA的变化规律。方法 采用原位杂交和反转录聚合酶链反应 (reversetranscriptionpolymerasechainreaction ,RT PCR)的方法 ,观察成年大鼠面神经切断和即刻端端吻合后面神经核trkB和trkCmRNA的时程变化。结果 面神经单纯切断组术后第 3日损伤侧面神经核trkBmRNA信号强度开始增加 ,7d增加最为明显 ,14d开始下降 ,但 2 1d与 35d损伤侧trkBmRNA信号强度仍高于未损伤侧。神经切断后trkC的变化与trkB相反。在面神经切断后端端吻合组 ,损伤侧面神经核trkB和trkCmRNA信号强度的变化趋势与单纯切断组基本相同 ,但吻合组trkB和trkCmRNA信号强度在术后 35d已恢复正常。RT PCR的结果与原位杂交结果基本一致。术后 2 1d和 35d面神经核trkB和trkC阳性条带相对密度在两组之间的差异具有显著性意义 (ttrkB ,2 1=13 795 ,ttrkC ,2 1=7 4 4 5 ,ttrkB ,3 5=8 5 6 0 ,ttrkC ,3 5=10 132 ,P <0 0 1)。结论 面神经损伤可引起面神经核运动神经元trkBmRNA升高 ,而trkCmRNA下降 ;面神经切断后即刻行端端吻合并不能影响神经损伤所诱导的trkB和trkCmRNA的变化 。

Objective To explore the changes of receptor tyrosine kinase B and C (trkB and trkC )mRNA in facial motoneurons following facial nerve injury and repair Methods The time course of trkB and trkC mRNA in facial motoneurons following facial nerve transection and anastomosis was analyzed using in situ hybridization(ISH) and reverse transcriptase polymerase chain reaction(RT PCR) in adult rats Results In the facial nerve simple transection group, the intensity of trkB mRNA signal began to increase to 3d post operation and to its maximum at 7d Then, the intensity started to decrease at 14d, but it was still higher than that in the contralateral side at 35d After facial nerve injury, the changing trend of trkC mRNA was in the contrary to that of trkB In the group of anastomosis, the changing trend of the intensity of trkB and trkC mRNA signal in the lesioned side was almost the same as that in the transection group However, the intensity of trkB and trkC mRNA signal in the lesioned side returned to normal level at 35d The finding obtained by RT PCR was consistent with that of ISH The statistic t test showed significant differences between the two groups for the relative density level of positive band for trkB and trkC at 21d?35d post operation, respectively, ( t trkB,21 =13 795, t trkC,21 =7 445, t trkB,35 =8 560, t trkC,35 =10 132, P <0 01) Conclusions Transection of the facial nerve results in a upregulation of trkB mRNA, but a downregulation of trkC mRNA in axotomized facial motoneurons The immediate anastomosis can′t counteract and attenuate the changes of trkB and trkC induced by the nerve injury, but whether the changes of trkB and trkC return to normal level depends on the regeneration facial nerve