It is generally accepted that nicotine affect learning ability and memory functions, especially during adolescence. c-Fos is an immediate early gene whose expression is sometimes used as a marker for stimulation-induced changes in the metabolic activity of neurons. The expression of c-Fos is induced by a variety of stimuli and expression of c-fos mRNA in hippocampal regions is used as a marker for neuronal activity. In the present study, the effect of dose-dependence of the nicotine on the c-Fos expression in the hippocampus of young rats was investigated via immunohistochemistry. From the present results, the number of Fos-positive cells in each region of the hippocampus was decreased following treatment with nicotine as dose-dependently. In addition, it appears that nicotine at low doses does not affect the level of apoptosis in the dentate gyrus of the hippocampus; in contrast, nicotine at high doses seems to enhance apoptosis in the dentate gyrus. Based on the results, it can be suggested that nicotine-induced suppression on Fos expression in the hippocampus of young rats may be an underlying mechanism of nicotine-induced disruption of information processing during the adolescence.
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