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目的 探讨慢性捆绑紧张对大鼠学习与记忆的影响及其可能的神经生物学机制。方法 选雄性 SD大鼠 18只 ,其中 10只为实验组 ,8只为对照组。对实验组采用捆绑器每天捆绑 6 h,2 1天后用 Y迷宫对两组大鼠进行行为检测 ,并用酶组织化学和免疫组织化学方法观察海马内一氧化氮合酶 (NOS)阳性神经元及 Tau蛋白 (Tau5 )免疫反应的变化。结果 1实验组大鼠学会躲避电击的次数为 35 .7± 7.5次 ,对照组为 2 5 .2± 2 .8次 ,P<0 .0 1;2海马右侧 CA1 区 NOS阳性神经元数目 ,对照组 2 7.2± 4.8个 ,实验组 38.9± 6 .4个 ,P<0 .0 5 ;NOS阳性神经元胞质平均灰度 ,对照组 170 .7± 11.8,实验组 16 2 .5± 12 .6 ,P<0 .0 5 ;3海马右侧 CA3 区 Tau5免疫阳性产物的平均灰度 ,对照组 16 1.7± 12 .8,实验组 145 .8± 13.8,P<0 .0 5。结论 一氧化氮产生过多而导致的神经毒性作用可能是慢性捆绑紧张导致动物学习与记忆功能受损的部分神经生物学机制 ,而海马 CA3 区神经元内所有的 Tau蛋白 (磷酸化及非磷酸化的 Tau)的总量增多说明 Tau蛋白的变化可能在此过程中起一定的作用。
Objective To investigate the effect of chronic binding stress on learning and memory in rats and its possible neurobiological mechanism. Methods 18 male SD rats were selected, of which 10 were experimental group and 8 were control group. The rats in the experimental group were tied for 6 h every day with bundlers, and the behavior of the two groups was detected by Y-maze after 21 days. The activity of nitric oxide synthase (NOS) positive neurons in the hippocampus was observed by enzyme histochemistry and immunohistochemistry Tau protein (Tau5) immune response changes. Results 1 The number of rats learned to avoid electric shock in experimental group was 35.7 ± 7.5 times and that in control group was 25.2 ± 2.8, P <0.01; 2 The number of NOS positive neurons in right CA1 of hippocampus 2 7.2 ± 4.8 in the control group, 38.9 ± 6.4 in the experimental group, P <0.05; mean gray value of the cytoplasm of NOS positive neurons was 170.7 ± 11.8 in the control group and 16 2 ± 5 in the experimental group 12.6, P <0.05; 3 The average grayscale of Tau5 immunopositive products in the CA3 region of the right hippocampus was 16 1.7 ± 12.8 in the control group and 145.8 ± 13.8 in the experimental group, P <0.05. Conclusions The neurotoxic effect caused by overproduction of nitric oxide may be a partial neurobiological mechanism of chronic binding stress in impaired learning and memory in animals. However, all Tau proteins in neurons of hippocampal CA3 region (phosphorylated and non-phosphorylated Tau) increase in total shows that changes in Tau protein may play a role in this process.