ALUMINUM TOXICITY IN A MOLLUSCAN NEURON: EFFECTS OF COUNTERIONS

Abstract

Previous studies using the freshwater snail Lymnaea stagnalis have indicated significant accumulation of aluminum (Al) from simple salts (chloride or nitrate) or Al lactate \[Al(lactate)₃] preparations, but not from the Al maltol complex \[Al(maltol)₃]. This is in contrast to findings in mammalian systems, where uptake and neurotoxicity are greatest for the soluble and lipophilic Al(maltol)₃ complex. This study was undertaken to investigate the direct effects of extracellular Al (100 muM) from three Al preparations \[AlCl₃, Al(lactate)₃ and Al(maltol)₃] on electrophysiological parameters of an identified neuron, the right parietal dorsal 1 (RPD1) neuron, of L. stagnalis in vitro. The effects of the corresponding counterion/ligand on the solubility and availability of Al in solution were also examined. Significant effects of Al on electrical properties, including membrane depolarization, 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 remained as the soluble monomeric complex. Qualitative differences were also observed between the response to AlCl₃and Al(lactate)₃, despite their similar chemistry. The extent of action potential broadening was greater with Al(lactate)₃, suggesting some interaction between Al and lactate in their cellular uptake and/or toxicity. It is suggested that polyhydroxy Al species are toxic to molluscan neurons, possibly via disruption of intracellular Ca²⁺ homeostasis.