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The present study was undertaken to assess age-related changes in the Purkinje's cells in the rat cerebellar cortex. The cellular and nucleolar volumes and the volume percentage of lipofuscin per cytoplasma were measured in six age groups. The number of Purkinje's cells was also counted. The cellular volume of rats aged 18, 24 and 30 months decreased significantly as compared with that of 3-month-old rats. The nucleolar volume of rats aged 12, 18, 24 and 30 months decreased significantly as compared with that of 3-month-old rats. The accumulation of lipofuscin in the cytoplasma of the Purkinje's cells was observed more or less in all ages. The degree of accumulation of lipofuscin in the Purkinje's cells increased with aging. The number of Purkinje's cells at the ages of 24 and 30 months decreased significantly as compared with that of 3-month-old rats.

Six age groups, each composed of four animals from each of the following ages, were used to assess age-related ultrastructural changes in the neuropil of the 111 layer of the frontal cortex in rats: 3, 6, 12, 18, 24 and 30 months old. Random samplings within the neuropil were taken to produce 40 electron micrographs in each rat (totaling 960). The profiles of axon terminals, dendrites and astroglial processes in the neuropil of each micrograph were traced. Then the percentage of their areas for the area of neuropil (relative volume fraction) was examined using the image analyzer system.The relative volume fractions of both the axon terminals and dendrites for the neuropil were found to have decreased in the aged rats. On the contrary, the relative volume fraction of astroglial processes for the neuropil had progressively increased with aging.

Dietary supplementation of fish oil containing eicosapentaenoic acid (C20:5 n-3, EPA) and docosahexaenoic acid (C22:6 n-3, DHA) has been shown to exert protective effects on ischemic/reperfused hearts. We determined whether deprivation of fish oil from the diet paradoxically enhances susceptibility of cardiomyocytes to hypoxia/reoxygenation-induced injury and whether supplementation with either EPA or DHA overcomes such alterations. Rats were fed with fish-oil-rich (FOR) diet, fish-oil-deprived (FOD) diet alone, FOD diet with EPA (1 g/kg/day), or FOD diet with DHA (1 g/kg/day) for 4 weeks. The FOD diet reduced n-3 polyunsaturated fatty acids (PUFAs) and increased n-6 PUFAs such as linoleic (C18:2) and arachidonic acids (C20:4) in myocardial phospholipids. EPA or DHA supplementation increased its incorporation into phospholipid pools. Cardiomyocytes isolated by treatment with collagenase were subjected to 150 min of hypoxia and subsequent reoxygenation for 15 min. In the FOD diet group, the number of surviving rod-shaped cells after hypoxia and reoxygenation was smaller than that of the FOR group. Supplementation with EPA did not affect the number of rod-shaped cells, but attenuated reoxygenation-induced reduction in the number of square-shaped cells. In contrast, DHA supplementation did not afford any protection. The results suggest that deprivation of fish oil from dietary intake enhances the susceptibility of cardiomyocytes to hypoxic injury, and EPA, but not DHA, is capable of salvaging cardiomyocytes from hypoxia/reoxygenation-induced damage.

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