| Budget Amount *help |
¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1993: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1992: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Research Abstract |
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.
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