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Study on Synaptic Plasticity in Aging Brain Tokyo Metropolitan Inst. Gerontology,

衰老大脑突触可塑性的研究东京都研究所

基本信息

批准号：
04836028
负责人：
ANDO Susumu
金额：
$ 1.22万
依托单位：
Tokyo Metropolitan Institute of Gerontology
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1992
资助国家：
日本
起止时间：
1992 至 1993
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-04836028/
关键词：
Aging Brain Synapse Plasticity Na K-ATPase Cholinergic Ganglioside

项目摘要

Dysfunction of aging brains is speculated to be accelerated by neuronal loss or diminished density of synapses. Three objectives of this study were as follows : 1. to examine the age-related changes of synaptic functions ; 3. to test whether the prevention of the decrement of synaptic density might retard the decreasing brain functions.We found significant decreases in resting membrane potential and in the activity of an electrogenic enzyme, Na/K-ATPase as a synaptic dysfunction in a previous work (Brain Res., 506 : 46-52, 1989). In this study, the cntent of Na/K-ATPase in synaptic membranes was proved to decrease in late senescence. Secondly, four new species of ganglioides were identified as neuronal membrane markers. Two of them were assigned as cholinergic neuron-specific antigens, Chol-1, and named GT1aalpha and GQ1balpha. Othe two were O-acetylated gangliosides, O-Ac-GT3 and O-Ac-GT2. The latter two were shown to be localized on the growth cone membranes of dendritic fibers. Thirdly, rat brains were demonstrated to greatly develop in rearing under enriched environment. Their cognitive functions such as memory and learning ability were better improved during maturation than control, and were maintained on a level with young stage during senescence. Quntitation of a synaptic marker protein, synaptophysin revealed that the synaptic density definitely increasedin enriched environmental group than in control. This may indicate the possibility that brain dysfunction due to aging could be prevented or retarded by increasing density of synapses.

据推测，衰老大脑的功能障碍会因神经元的丧失或突触密度的降低而加速。本研究的目的如下：1.研究突触功能的增龄性变化; 3.为了测试防止突触密度的减少是否可以延缓脑功能的降低，我们发现静息膜电位和产电酶Na/K-ATP酶活性的显著降低是先前工作中的突触功能障碍（Brain Res.，506：46-52，1989）。本研究证实了突触膜Na/K-ATP酶的含量在衰老后期下降。其次，鉴定了四种新的神经节样细胞作为神经元膜标记。其中两个被指定为胆碱能神经元特异性抗原，Chol-1，并命名为GT 1a α和GQ 1a α。另外两种为O-乙酰化神经节苷脂O-Ac-GT 3和O-Ac-GT 2。后两者被证明是本地化的树突状纤维的生长锥膜上。第三，在丰富的环境下饲养大鼠，大脑得到了极大的发展。成熟期的记忆、学习等认知功能较对照组有明显提高，衰老期的记忆、学习等认知功能基本保持在幼年期水平。突触标志蛋白突触素的定量分析显示，丰富环境组的突触密度明显高于对照组。这可能表明，增加突触的密度可以防止或延缓衰老引起的脑功能障碍。