| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1994: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1993: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Research Abstract |
In order to verify whether active oxygen species actually attack nervous systems and make the oxidative injury, resulting in the deterioration of the physiological functions in nerve terminals, and whether the deterioration is correlated with brain aging, we investigated the effect of peroxide on the functions of nerve terminal in rats which were exposed by 100% oxygen atmosphere. Results obtained as follows :
Through oxidative stress, the morphological changes ; i.e.swelling of astrocytes around the vessels, deformation of nuclei of nerve cells, mitochondrial swelling, and the abnormal accumulation of synaptic vesicles in the terminals were observed. Release of acetylcholine from the terminal through the stimulation of veratridine was significantly decreased. The membrane permeability to glucose was increased and the fluidity was decreased by oxygen exposure and with aging. The content of lipid peroxide in the membranes was higher than that of the unexposed rats, and the content of unsaturated fatty acids, especially arachidonic acid and docosahexaenoic acid was significantly decreased. Although catalase and glutathione peroxidase activities were increased, Superoxide dismutase activity was decreased by oxygen exposure and with aging.
On the basis of these findings, it was thought that active oxygen species may attack the nerve terminals, and hence, peroxidize the synaptic membranes, resulting in deterioration of synaptic membranes.
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