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CHANGE IN SPATIAL MEMORY AND HIPOCAMPAL EXPRESSION OF C-FOS PROTEIN AS A RESULTS OF IMPAIRED MASTICATION IN THE SENSCENCE-ACCELERATED MOUSE

感觉加速小鼠咀嚼功能受损导致空间记忆和海马 C-FOS 蛋白表达的变化

基本信息

批准号：
09832012
负责人：
NISHIYAMA Katsuhiro
金额：
$ 1.92万
依托单位：
Kanagawa Dental College
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1997
资助国家：
日本
起止时间：
1997 至 1998
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-09832012/
关键词：
Hippocampal mastication oncogene MRI c-Fos Morris water maze human brain derived factor 記憶アセチルコリン神経

项目摘要

In the present study, we evaluated the effect of reduced mastication on the neuronal mechanism responsible for age-related memory impairment, by examining the effects of the cutting off of the upper molars (molarless) on hippocampal expression of c-fos protein (c-Fos) and spatial memory in the senescence-accelerated mouse (SAM-P8) and the senescence-resistant mouse (SAM-R1). In the Morris water maze test, the escape latency for intact SAM-P8 to find the hidden platform was longer in the first several days and thereafter almost the same as that for the SAM-R1 control. Immunohistochemical analysis following this behavioral test (on day 10) revealed no significant density of c-Fos-immunopositive cell nuclei in the hippocampal formation between these two groups. However, in molarless SAM-P8, both a marked increase in escape latency in the water maze and a significant decrease in c-Fos-immunoposive nuclei density were seen, the greatest effect being found in the CAl subfield, followed by the CA3 subfield, then the dentate gyrus. These changes became more pronounced with the increasing duration of the molarless condition. In contrast, the molarless SAM-R1 did not show any significant changes in maze leaning and c-Fos expression. Furthermore, the molarless condition had no effect on GFAP-positive cell density in the hippocampal formation in either SAM-R1 or SAM-PS mice. These results suggest that impaired mastication may cause the age-related reduction in hippocampal activity, linked to impairment of memory.

在本研究中，我们评估咀嚼减少的神经机制负责与年龄相关的记忆障碍的影响，通过检查切断上磨牙（无磨牙）对海马c-Fos蛋白（c-Fos）的表达和空间记忆的快速老化小鼠（SAM-P8）和抗衰老小鼠（SAM-R1）。在Morris水迷宫实验中，完整SAM-P8寻找隐藏平台的逃避潜伏期在最初几天较长，此后几乎与SAM-R1对照相同。免疫组织化学分析后，这一行为测试（在第10天）显示没有显着密度的c-Fos免疫阳性细胞核在这两组之间的海马结构。然而，在无磨牙SAM-P8中，在水迷宫中的逃避潜伏期显著增加，c-Fos免疫阳性核密度显著降低，在CA 1子区中发现最大的影响，其次是CA 3子区，然后是齿状回。这些变化变得更加明显的无磨牙条件的持续时间增加。相比之下，无磨牙SAM-R1在迷宫学习和c-Fos表达方面没有显示出任何显著变化。此外，无磨牙条件对SAM-R1或SAM-PS小鼠海马结构中GFAP阳性细胞密度没有影响。这些结果表明，咀嚼受损可能会导致海马活动的年龄相关性降低，与记忆障碍。