Differentiated neuroblastoma cells are more susceptible to aluminium toxicity than developing cells.

The influence of aluminium (20-50 micrograms/ml) on neuronal function was examined using electrophysiological techniques and neuroblastoma clone cells which offer a convenient model of differentiating and fully active neurons. Two specific questions were addressed: 1) Can differentiated cells maintain their normal excitable function when exposed to aluminium? 2) Can proper development of electrophysiological properties be achieved in its presence? We report that aluminium caused premature onset of deterioration in fully differentiated cells. Within 4-6 days they depolarized from -29.3 +/- 0.9 mV to levels lower than -15 mV; compound polyphasic action potentials were gradually replaced by slow monophasic spikes before the final loss of excitable properties and structural deformations was noticed. Developing cells followed the normal pattern of differentiation in the presence of aluminium: within 7 days they extended neurites, hyperpolarized and exhibited polyphasic spikes. These results show that neuroblastoma cells are apparently less susceptible to aluminium's toxicity during the process of development than after differentiation. Possible mechanisms by which aluminium may exert its effects are discussed in view of these observations.