Protective role of lithium during aluminium-induced neurotoxicity

The present study was designed to examine the protective potential of lithium if any in ameliorating the alterations induced by aluminium (Al) on behavioral and neurochemical indices. Al was given orally (100 mg/kg b.wt./day) whereas lithium was administered through diet (1.1 g/kg diet) to rats for a total duration of 2 months. Active and passive avoidance tests revealed significant alterations in the short-term memory and cognitive behavior in rats treated with AI. Further, locomotor as well as muscular activities were also found to be significantly affected. Co-administration of lithium with AI caused significant improvement in the short-term memory, cognition, anxiety, locomotion and muscular activity. Further, Al exposure led to a significant decrease in the acetylcholinesterase activity in both the cerebrum and cerebellum. Monoamine oxidase enzyme activity was significantly increased in cerebrum whereas a decrease was observed in cerebellum after Al treatment. Dopamine and serotonin levels were also found to be significantly decreased but the levels of reactive oxygen species were significantly increased in both the regions following AI treatment. Lithium supplementation to Al treated animals caused a significant improvement in the activities of enzymes acetylcholinesterase and monoamine oxidase which were altered by Al. Further, lithium when given along with Al was also able to regulate the levels of dopamine, serotonin and reactive oxygen species in both the regions and the values were found close to the normal controls. Ultrastructural studies revealed alteration in the structure of synapse after Al treatment. Therefore, the study strengthens the hypothesis that lithium can be used as a neuroprotectant during AI induced neurotoxicity. (C) 2009 Elsevier Ltd. All rights reserved.