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The present study was designed to assess the influence of long term L-deprenyl treatment on some microanatomical parameters of aging rat frontal cortex and hippocampus. Male Sprague-Dawley rats of 19 months of age were divided into three groups. Rats of the first group received an oral daily dose of 1.25 mg/kg L-deprenyl; animals of the second group were treated with an oral daily dose of 5 mg/kg L-deprenyl, whereas rats of the third group were left untreated and used as control. Treatment lasted for 5 months, and rats were sacrificed at 24 months. At this age they were considered to be old. Another group of 11-month-old rats was used as an adult reference group. The density of nerve cell profiles and of glial fibrillary acidic protein (GFAP) immunoreactive astrocytes was decreased and increased respectively in the frontal cortex and in the different portions of the hippocampus in old in comparison with adult rats. A decrease in the intensity of sulfide silver staining in the mossy fibers of the hippocampus was also observed in old rats. Moreover, a cytoplasmatic accumulation of lipofuscin was noticeable in old rats as well as a significant increase of the monoamine-oxidase (MAO) B reactivity both in the frontal cortex and in the hippocampus. A higher density of nerve cell profiles, of sulfide silver staining, and fewer astrocyte profiles were noticeable in the frontal cortex and in the hippocampus of old rats treated with 5 mg/kg/day of L-deprenyl. This dose of the compound also significantly reduced lipofuscin accumulation and MAO-B reactivity in old rats. However, the lower dose of the compound did not cause any statistically significant effect on the microanatomical parameters investigated with the exception of sulfide silver staining and lipofuscin accumulation, which were increased and decreased respectively after 1.25 mg/kg per day of L-deprenyl. The above results suggest that long-term treatment with L-deprenyl is able to counter some microanatomical changes typical of the aging frontal cortex and hippocampus in the rat. These changes seem to be in part related to the MAO-B inhibitory activity of L-deprenyl.
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