HgCl2 potentiates GABA activated currents in Lymnaea stagnalis L. neurones

Using the concentration clamp technique the effects of inorganic mercury (HgCl2) on gamma-aminobutyric acid (GABA) activated Cl- currents were studied on Lymnaea neurons. Hg2+ at concentrations of 0.01-1 microM caused a significant increase in the GABA induced chloride permeability of the cell membrane. With simultaneous application of GABA and 0.1 microM Hg2+ the amplitudes of the GABA activated inward Cl- currents were increased to a mean of 168%. The threshold concentration for potentiation was 0.01 microM Hg2+, while the GABA induced Cl- current was suppressed at concentrations higher than 100 microM. HgCl2 was also effective in decreasing the time-to-peak value and the time of inactivation of the GABA evoked Cl- current. In the presence of 0.1 microM mercury chloride the peak reached the maximum 1.6 times faster than without mercury. The effect was independent of the membrane potential, and mercury did not change the reversal potential of the GABA activated Cl- current. Application of mercury alone at concentrations effective to enhance GABA evoked Cl- permeability caused no or only a very small sustained inward current. However, higher mercury concentrations or repeated mercury application greatly increased the membrane permeability, and this effect could not be reversed by a 15 min wash. The results suggest, that low mercury concentrations act on GABA-ergic synapses at a postsynaptic site, and the potentiation of the ligand gated Cl- current may be an important factor in the mechanism of Hg2+ neurotoxicity.