老年性记忆减退大鼠内侧隔核-斜角带胶质纤维酸性蛋白过度表达

为探讨胶质纤维酸性蛋白 ( glial fibrillary acidic protein,GFAP)表达与一氧化氮合酶 ( nitric oxide synthase,NOS)神经元损伤引起的老年性记忆减退之间的关系 ,选用青年大鼠 2 0只 ,老年大鼠 40只 ,进行 Morris水迷宫行为学测定 ,将老年大鼠分为老年性记忆正常组 (简称正常组 )和老年性记忆减退组 (简称减退组 )。用免疫细胞化学、还原型烟酰胺腺嘌呤二核苷酸( nicotinamide adenine dinucleotide phosphate diaphorase,NADPH-d)组织化学及其双重反应分析内侧隔核 -斜角带 ( Septummedialis-Diagonal Band,SM-DB)中 GFAP和 NOS的表达。GFAP免疫细胞化学染色见老年大鼠 SM-DB中星形胶质细胞肥大 ,减退组大鼠更为明显。减退组平均胞体面积明显大于正常组 ( P<0 .0 1) ,胞体体密度明显高于正常组和青年组 ( P<0 .0 1) ;细胞的体密度也较正常组和青年组明显增加 ( P<0 .0 1)。GFAP免疫细胞化学和 NADPH-d组织化学双重反应可见减退组大鼠 SM-DB星形胶质细胞明显肥大 ,突起粗壮弯曲 ,GFAP超量表达 ,而 NOS阳性神经元数量减少 ,胞体变形 ,突起减少 ,着色的深度下降。提示引起老年性记忆减退的 NOS神经元损伤与 GFAP的过度表达有密切联系

OVEREXPRESSION OF GLIAL FIBRILLARY ACIDIC PROTEIN IN SEPTUM MEDIALIS-DIAGONAL BAND OF SENILE MEMORY DEFICITS RAT

For exploring the relationship of glial activity and senile memory deficits induced by NOS neuron insults, 60 male healthy SD rats (20 young and 40 old) were examined with Morris water maze. The old were divided into senile memory deficits rats (SMD) and senile memory normal rats(SMN). The overexpression of GFAP and astroglia hypertrophy were seen in septum medialis diagonal band(SM DB) of SMN, and more obviously in that of SMD. There was significant increase of numerical density in SM DB of SMD comparing with that of the young. Average area, somata volume density and cell volume density of astroglia of SMD were increased significantly in comparison with that of SMN and the young. In the GFAP immunochemistry and NADPH d histochemistry double stained SMD preparation GFAP was overexpressed and NOS neurons decreased, distorted and pale, the glia obviously hypertrophied, and their dendrites robust and winding. The glia of SMN hypertrophied slightly, while neurons were not occur degenerated. The changes in SM DB of SMD may reflect a sustained upregulation of glial activity with the insults of neurons, which induced memory deficits. (Figures 1～6 on plate 3)