Objective    To study the neurotoxicity of chronic aluminum overload and the protective effects of nimodipine in rats.     Methods    The brain damage models of rats were established via intragastric administration of aluminum gluconate（element aluminum 400 mg/kg） once a day

5 d/week for 12 weeks. The step-down test and programmed Morris water maze test were used to evaluate the changes of learning and memory functions of rats.  Pathomorphological changes of hippocampi of rats were observed.  The activities of SOD

ChAT

AchE

MAO-B and the contents of MDA of brain tissue in rats were also measured.  Nimodipine (80 mg/kg) were intragastrically administered 4 h after aluminum administration every time for 12 weeks.      Results    Chronic aluminum administration induced the impairment of avoidance learning and memory ability and spatial oriental ability.  Consistent with the behavioral changes

neuronal death in the hippocampi

decreased activities of SOD and ChAT

increased content of MDA

and increased activity of MAO-B and AchE were detected in the aluminum-overload mice.  The administration of nimodipine could significantly protect rats from the brain damage

and behavioral and biochemical changes above caused by aluminum overload were in a dose-dependent manner.     Conclusion    These results suggest that changes of cellular calcium overload and oxide stress and   MAO-B activities are involved in pathophysiological mechanisms of brain injury induced by chronic aluminum overload.  Nimodipine has a protective effect on neurotoxicity of chronic aluminum overload.