Aluminum toxicity in a molluscan neuron: Effects of counterions

Previous studies using the freshwater snail Lymnaea stagnalis have indicate d significant accumulation of aluminum (Al) from simple salts (chloride or nitrate) or Al lactate [Al(lactate)(3)] preparations, bur not from the Al m altol complex [Al(maltol)(3)]. This is in contrast to findings in mammalian systems, where uptake and neurotoxicity are greatest for the soluble and l ipophilic Al(maltol)(3) complex. This study was undertaken to investigate t he direct effects of extracellular Al (100 mu M) from three Al preparations [AlCl3, Al(lactate)(3) and Al(maltol)(3)] on electrophysiological paramete rs of an identified neuron, the right parietal dorsal 1 (RPD 1) neuron, of L. stagnalis in vitro. The effects of the corresponding counterion/ligand o n the solubility and availability of Al in solution were also examined. Sig nificant effects of Al on electrical properties, including membrane depolar ization, increased firing activity, and abnormal firing patterns, were seen in the presence of AlCl3 and Al(lactate)(3), which formed polyhydroxy and labile Al species in aqueous solution, but not with Al(maltol)(3), which re mained as the soluble monomeric complex. Qualitative differences were also observed between the response to AlCl3 and Al(lactate)(3), despite their si milar chemistry,. The extent of action potential broadening was greater wit h Al(lactate)(y) suggesting some interaction between Al and lactate in thei r cellular uptake and/or toxicity. It is suggested that polyhydroxy Al spec ies are toxic to molluscan neurons, possibly via disruption of intracellula r Ca2+ homeostasis.