Action of lead on glutamate-activated chloride currents in Helix pomatia L. neurons.
1. In molluscan neurons glutamate may, on different neurons, evoke either excitation or inhibition. We studied neurons of Helix pomatia which have hyperpolarizing responses to glutamate and determined the effects of lead on these responses. 2. In voltage clamp experiments, the reversal potentials of these glutamate responses indicate that they are due to a conductance increase to chloride ions. Further evidence for this conclusion was obtained by the demonstration that responses to glutamate remained unaffected in experiments with intracellular dialysis with K-free saline in the presence of Na- and K-free extracellular media. In these circumstances, there is effectively no other ion than chloride to carry the current. In isolated neurons the glutamate-evoked chloride current is concentration dependent between 25 and 2500 microM. The current rises over 200 msec and declines in the continued presence of glutamate over a period of about 3 sec. 3. Lead (0.5-1.0 microM) potentiated the glutamate-evoked chloride current provided that the channels were not maximally activated. The potentiation was greater if lead was added 30-60 sec before glutamate application. 4. These results suggest that potentiation of transmitter-evoked responses by lead must be considered as yet another possible site of action of lead on neurons, and thus this effect must be considered as a part of the mechanism responsible for the neurotoxicity of this heavy metal.