淋巴滞留脑病模型大鼠内侧隔核-斜角带垂直支一氧化氮合酶神经元的改变

目的 :探讨淋巴滞瘤脑病模型大鼠内侧隔核 斜角带垂直支 (Septummedialis verticaldiagonalbandcomplex ,SM vDB)神经元一氧化氮合酶 (Nitricoxidesynthase,NOS)表达与空间参考记忆变化的相关性。方法 :用免疫细胞化学方法显示记忆获得后及淋巴滞留脑病期间 ,大鼠SM vDB的NOS阳性神经元 ,并进行定量分析。结果 :(1 )训练组阳性神经元数比对照组分别增加 96.91 % ,62 .96% (P <0 .0 1 ) ,与逃避潜伏期呈明显负相关 (SMr=-0 .7646,P <0 .0 1 ;vDBr=-0 .81 5 2 ,P <0 .0 1 ) ;细胞面积分别增加 42 .5 1 % ,3 5 .0 0 % (P <0 .0 1 ) ;免疫反应灰度值分别增加1 3 0 .5 1 % ,1 1 5 .41 % (P <0 .0 1 )。 (2 )脑病模型组与假手术组相比 ,阳性神经元数量分别减少 2 5 .91 % ,2 0 .1 3 % (P <0 .0 1 ) ,与逃避潜伏期呈明显负相关 (SMr=-0 .65 3 8,P <0 .0 1 ;vDBr=-0 .72 42 ,P <0 .0 1 ) ;细胞面积分别减少1 4.92 % ,1 2 .97% (P <0 .0 1 ) ,免疫反应灰度值分别减少 3 3 .3 4% ,41 .5 4% (P <0 .0 1 )。结论 :淋巴滞留性脑病神经元NOS表达减少 ,可能损害空间参考记忆的保持

Changes of NOS neurons in septum medialis vertical diagonal band complex of iymphostatic encephalopathy rat

Objective:To explore the correlation ship between the nitric oxide synthase(NOS) neurons in the septum medialis vertical diagonal band complex(SM vDB) of lymphostatic encephalopathy (LSEP) rat and the spatial reference memory. Methods: The changes in NOS ir neurons in SM vDB from both acquired memory and LSEP rat were demonstrated with immunocytochemical method quantitatively. Results: (1)Comparing with the control, the number of NOS ir neurons in SM vDB from trained group increased by 96.91%, 62.96%(P<0.01), with a negative correlation between the mean escape latency and the counts of NOS ir neuron in SM vDB(SM r=-0.7646, P<0.01; vDB r=-0.8152, P<0.01). The somata increased by 42.51%, 35.00%(P<0.01), and the gray level by 130.51%, 115.41%(P<0.01). (2)Comparing with the sham, memory retention of the LSEP model was impaired, the number of NOS ir neurons in SM vDB of the model decreased by 25.91%, 20.13%(P<0.01), with a negative correlation between the mean escape latency and the counts of NOS ir neuron in SM vDB(SM r=-0.6538,P<0.01; vDB r=-0.7242,P<0.01). The somata area decreased by 14.92%, 12.97%(P<0.01), and the gray level by 33.34%, 41.54%(P<0.01). Conclusion: The decrease of NOS ir neurons may damage the spatial reference memory retention in LSEP.