ALUMINUM IMPAIRS HIPPOCAMPAL LONG-TERM POTENTIATION IN RATS IN-VITRO AND IN-VIVO

Although aluminum (Al) contributes to a variety of cognitive dysfuncti ons and mental diseases, the underlying mechanisms of Al interactions with the nervous system are still unknown. We have studied the action of Al on synaptic transmission and long-term potentiation (LTP) by per forming electrophysiological recordings both in vivo, using freely mov ing animals, and in vitro, using hippocampal slices. In vivo recording s of the population spikes (PSs) of dentate gyrus granule cells in res ponse to medial perforant path stimulation were performed on both acut ely and chronically (Al each day for 5 days) intraventricularly inject ed animals. Acute Al-infusion (calculated brain concentrations of 0.27 , 0.68, and 2.7 mu g/ml) had no influence on baseline values. Al at 0. 27 mu g/ml did not alter the induction and maintenance of LTP, but 0.6 8 and especially 2.7 mu g/ml Al lead to a reduction in LTP, and the po tentiation declined to baseline within 2 h. In chronic animals their n euronal responsiveness was reduced and in 30% of the rats the PS was c ompletely lost. High-frequency tetanization failed to induce LTP. In s lices, field potentials were evoked stimulating Schaffer collaterals a nd recording pyramidal cells of the CA1 region. Bath application of 0. 68 mu g/ml Al increased the baseline amplitude of the PS slightly, whe reas 2.7 mu g/ml decreased the amplitude and concentrations >5.4 mu g/ ml blocked the PS completely. Induction of LTP in the presence of 0.68 mu g/ml Al led to a smaller increase of the PS amplitude compared to controls, but the duration of LTP was not affected. In the presence of 2.7 mu g/ml Al LTP was further reduced and declined to baseline level s within 60 min. Given that LTP is a form of synaptic plasticity under lying some forms of learning, our data suggest that both preparations are suitable models for investigating actions of Al-induced neurotoxic ity. (C) 1995 Academic Press, Inc.