产前束缚应激下调子代大鼠海马生长相关蛋白43的表达

目的：通过检测产前束缚应激子代大鼠脑内海马中生长相关蛋白（GAP-43）的表达，探讨该应激降低大鼠空间学习记忆能力的原因。方法：选用SD大鼠20只，正常饲养7d，使其怀孕，并完全随机分为应激组（n=10）和对照组（n=10），在母鼠怀孕的13～19d，白天使母鼠钻入一直径7cm，长19cm的圆柱形容器中，实施束缚应激。对照组则正常饲养。待母鼠生产后，于仔鼠出生后1、7和30d时将其处死．取脑组织应用Western Blotting方法检测海马中GAP-43的表达。均有显著性．另外30d两组在处死前先进行Morris水迷宫实验。结果：Morris水迷宫实验中，应激组与对照组相比，寻找站台的潜伏期有明显的延长（P〈0．05）。策略方面，应激组多选择随机式，对照组多选择直线式，差异有统计学意义（P〈0．05）。仔鼠应激组脑海马GAP-43的表达在1和7d高于对照组，在30d时低于对照组（P〈0．叭）。结论：产前束缚应激刺激早期可使GAP-43反应性升高，但长期看，会下调子代大鼠脑海马GAP-43的表达，使神经元轴突发育异常．最终导致子代大鼠认知缺损。

Prenatal restraint stress down-regulates GAP-43 expression in hippocampus of filial rats

Objective：To examine the GAP-43 expression in hippocampus of offspring of rats subjected to prenatal restrain stress, and to explore the factors associated with lowered spatial learning and memory capability in rats. Methods： Twenty SD rats were selected and normally bred for 7d so as to be adapt to the new surroundings. Then the female rats were impregnated and randomized into prenatal stress （PS） group and normal control group. Prenatal restraint stress was performed by forcing the female rats of PS group into a cylindrical container （7 cm by diameter and 19 cm by length in the daytime） during 13 d to 19 d of pregnancy,while the normal control group remained normally bred. After birth, the filial rats were sacrificed at 1 d, 7 d and 30 d. Brain tissues were obtained and detected for GAP-43 expression in hippocampus by Western blotting. In addition,30-day-old offspring were subjected to Morris water maze test before sacrifice. Results： In Morris water maze, the PS group had significantly prolonged latency in finding the platform as compared with the normal control group （P 〈 0.05 ）. As regards to search strategies, random pattern was used more frequently in PS group, contrasted with linear pattern in the normal control group （ P 〈 0.05 ）. Compared with the normal control group, PS group had higher level of GAP-43 expression at ld and 7d but lowered expression at 30 d （P 〈 0.01 ）. Conclusion ： Prenatal restraint stress may increase the reactivity of GAP-43 at early stage, But over a long time, it may down-regulate GAP-43 expression in the hippocampus of filial rats, hence abnormal development of neuron axons and consequently cognitive impairment in these rats.