Extracellular Ca(2+) modulation of triethyltin neurotoxicity in area CA1 of the rat hippocampal slice.
The present study examined the possible role of extracellular Ca(2+) in triethyltin (TET) neurotoxicity in area CA1 of the rat hippocampal slice. Slices were exposed to 20 mum-TET-Br for 30 min in an environment of normal or no extracellular Ca(2+), and were then monitored for 4 hr post-exposure. In a normal Ca(2+) 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 Ca(2+)-free environment, however, the same TET exposure led to rapid tissue death following the onset of TET exposure. Thus, extracellular Ca(2+) decreased the apparent neurotoxicity of TET observed in a Ca(2+)-free environment. The results suggest that extracellular Ca(2+) 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 Ca(2+) environment and tissue death in a Ca(2+)-free environment remain to be elucidated.
Ting
Y L
YL
Department of Neurobiology, Northeastern Ohio Universities College of Medicine, Rootstown, OH 44272, USA.
Fountain
S B
SB
Teyler
T J
TJ