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Parkinson-\nlike syndrome, motor deficit, disturbed psychomotor development \nare typical signs of neuropathological alterations due to Mn in \nhumans. Methods: Young adult rats, in three groups of 16 each, \nreceived 15 and 59 mg/kg b.w. MnCl2, (control: distilled water) \nvia gavage for 10 weeks, and were kept for further 12 weeks. \nCorrelation of MnCl2 exposure to body and organ weights, \nneurobehavioral effects (spatial memory, exploratory activity, \npsychomotor performance, pre-pulse inhibition), and \nhistopathological changes (gliosis) was sought. Results: By the \nend of treatment, Mn accumulated in blood, cortex, hippocampus, \nand parenchymal tissues. Body and organ weights were reduced in \nhigh dose rats. All treated rats showed hypoactivity, decreased \nmemory performance, and diminished sensorimotor reaction. In the \ndentate gyrus of these, GFAP immunoreactivity increased. During \nthe post-treatment period, body weight of the high dose group \nremained decreased, locomotor activity returned to control, but \nthe lasting effect of MnCl2 could be revealed by amphetamine. \nConclusion: Using complex methodology, new data were obtained \nregarding the relationship between the long-term effects of \nMnCl2 at neuronal and behavioral level. 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