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 sli ce. 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 p opulation excitatory post-synaptic potentials (EPSPs) by 95 min post-e xposure, and no recovery was observed following washout of TET. This d irect effect of TET on neurotransmission occurred without changes in t he conductive properties of the presynaptic Schaffer collaterals; the amplitude of population afferent fibre volley potentials remained stab le. In a Ca2+-free environment, however, the same TET exposure led to rapid tissue death following the onset of TET exposure. Thus, extracel lular Ca2+ decreased the apparent neurotoxicity of TET observed in a C a2+-free environment. The results suggest that extracellular Ca2+ modu lates TET neurotoxicity, manifested as suppression of synaptic potenti als, in area CA1 of the hippocampal slice. However, the mechanisms und erlying TET-induced suppression of evoked synaptic potentials in a nor mal Ca2+ environment and tissue death in a Ca2+-free environment remai n to be elucidated.