Effects of chronic aluminum exposure on memory through multiple signal transduction pathways

Objective: To investigate the effects of chronic aluminum (Al) exposure on memory of rats by recording long-term potentiation (LTP) induction in CA1 region of Schaffer collateral (SC) of hippocampus and observing the changes of key LIP induction-related kinases. Methods: Forty weaned Wistar rats were divided into 4 groups ad libitum, each group 10 rats. Three groups were fed with 0.2%, 0.4% and 0.6% AlCl3 in drinking water for three months individually to set up the aluminum exposure models and the rest group was the control. After behavioral test, electrophysiological recordings were made at area CA1 from hippocampal SC branch followed by biochemical examination for several key kinases involved in LTP induction and formation. Results: Chronic exposure of AI significantly decrease the activities of protein kinase C (PKC) and mitogen-activated protein kinase (MAPK) and reduced the expression levels of extracellular signal-regulated kinases (ERK1/2) and Ca2+-calmodulin dependent protein kinase II (CaMKII) in hippocampus, attenuating the population spike (PS) amplitude of LIP from the hippocampal CA1 region, causing impaired memory abilities of rats. Conclusions: Aluminum accumulation in the hippocampus affects several crucial kinases involved in LIP induction and formation, resulting in impairment of memory. (C) 2010 Elsevier B.V. All rights reserved.