神经生长因子对痴呆模型鼠海马突触素的影响

EFFECT OF NERVE GROWTH FACTOR ON SYNAPTOPHYSIN IN HIPPOCAMPUS OF AGED RATS WITH FIMBRIA-FORNIX TRANSECTION

切断SD老年鼠(24月龄)左侧穹窿海马伞.造成隔海马胆碱能系统损害的痴呆模型. 用免疫组化和图像分析技术分析神经生长因子对痴呆鼠海马突触素的影响.实验证明损伤一个月后.损伤对照组损伤侧海马CAI区多形层、辐射层、腔隙分子层和齿状回分子层突触素含量分别是减少了28.17% 、32.15%、17.36%和35.22%:NGF治疗组、损伤侧海马CAI区多形层、辐射层、腔隙分子层和齿状回分子层突触素含量只减少了6.17%、5.52%、13.50%和3.81%.提示神经生长因子能够促使痴呆鼠海马内突触素含量的增多.

ged male SD rats were subjected to left fimbria-fornix transection and received continuous infusion of NGF or CytC into the cerebroventricular space. On the 30th post-lesion day, brains were processed for synaptophysin immunocytochemistry. In the present study, we usedcomputer-assisted optical density measurements of synaptophysin immunostaining. The results were as follows: 30 days after unilaterally fimbria-fornix transection there was a significant decrease in the staining density. The value of COD decreased to 71. 53%, 67. 54%, 52. 64% and 64. 78% respectirely in the Oriens, Radiatum, Lacunosum and the molecular lay of dentate gyrus (MDG). Following the infusion of NGF, the value of COD went up to 93. 83%, 94. 48%, 86. 5% and 96.19% respectively in the Oriens, Radiatum Lacunosum and the MDG. The findings indicated that NGF reversed axotomy-induced decrease of synaptophysin of hippocampus.