EXTRACELLULAR CA2+ MODULATION OF TRIETHYLTIN NEUROTOXICITY IN AREA CA1 OF THE RAT HIPPOCAMPAL SLICE

The present study examined the possible role of extracellular Ca2+ in triethyltin (TET) neurotoxicity in area CA1 of the rat hippocampal slice. Slices were exposed to 20-mu-M-TET-Br for 30 min in an environment of normal or no extracellular Ca2+, and were then monitored for 4 hr post-exposure. In a normal Ca2+ environment, TET exposure suppressed population excitatory post-synaptic potentials (EPSPs) by 95 min post-exposure, and no recovery was observed following washout of TET. This direct effect of TET on neurotransmission occurred without changes in the conductive properties of the presynaptic Schaffer collaterals; the amplitude of population afferent fibre volley potentials remained stable. In a Ca2+-free environment, however, the same TET exposure led to rapid tissue death following the onset of TET exposure. Thus, extracellular Ca2+ decreased the apparent neurotoxicity of TET observed in a Ca2+-free environment. The results suggest that extracellular Ca2+ modulates TET neurotoxicity, manifested as suppression of synaptic potentials, in area CA1 of the hippocampal slice. However, the mechanisms underlying TET-induced suppression of evoked synaptic potentials in a normal Ca2+ environment and tissue death in a Ca2+-free environment remain to be elucidated.