Abstract
Blocking of the GABA-activated chloride current by cadmium was investigated in identified nerve cells (RPeD1, RPaD1) of the pond snail ( Lymnaea stagnalis L.), using a two-microelectrode voltage-clamp technique. Cd 2+, at 50 μM extracellular concentration, inhibited GABA-activated chloride currents, both in normal and Ca 2+-free solution. Intracellular injection of Ca 2+ or the application of caffeine mimicked the inhibitory effect of Cd 2+ on GABA-elicited currents. Cd 2+-block was eliminated, or it was substantially decreased, when neurons were intracellularly loaded with EGTA, or when the Ca 2+-release was blocked by ruthenium red. The blocking effect of Cd 2+ was also eliminated by applying G-protein inhibitors: pertussis toxin, suramin or GTP-γ-S. Finally, intracellularly injected Cd 2+ was ineffective at eliciting an inward current on GABA-activated currents, suggesting that the Cd 2+-binding site resides extracellularly. These results suggest that cadmium inhibited GABA-activated chloride currents by increasing the intracellular Ca 2+ level, by releasing it from intracellular stores and by interacting with a putative G-protein-coupled cell-surface “metal-receptor”.
Published Version
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