HGCL2 POTENTIATES GABA ACTIVATED CURRENTS IN LYMNAEA-STAGNALIS L NEURONS

Using the concentration clamp technique the effects of inorganic mercu ry (HgCl2) an gamma-aminobutyric acid (GABA) activated Cl- currents we re studied on Lymnaea neurones. Hg2+ at concentrations of 0.01-1 mu M caused a significant increase in the GABA induced chloride permeabilit y of the cell membrane. With simultaneous application of GABA and 0.1 mu M Hg2+ the amplitudes of the GABA activated inward Cl- currents wer e increased to a mean of 168%. The threshold concentration for potenti ation Was 0.01 mu M Hg2+, while the GABA induced Cl- current was suppr essed at concentrations higher than 100 mu M. 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 mu M mercury chlor ide the peak reached the maximum 1.6 times faster than without mercury . The effect was independent of the membrane potential, and mercury di d not change the reversal potential of the GABA activated Cl- current. Application of mercury alone at concentrations effective to enhance G ABA evoked Cl- permeability caused no or only a very small sustained i nward current. However, higher mercury concentrations or repeated merc ury application greatly increased the membrane permeability, and this effect could not be reversed by a 15 min wash. The results suggest, th at low mercury concentrations act on GABA-ergic synapses at a postsyna ptic site, and the potentiation of the ligand gated Cl- current may be an important factor in the mechanism of Hg2+ neurotoxicity.