The role of G proteins in the activity and mercury modulation of GABA-induced currents in rat neurons.

The role of G proteins in the functional modulation and potentiation by mercury chloride of the GABA(A) receptor-channel complex in rat dorsal root ganglion neurons was studied by using the whole-cell patch clamp technique. Stimulation of Gs proteins by application of GTP-gamma-S in the patch pipette or by incubation of neurons with cholera toxin reduced GABA-induced currents, suggesting modulation of GABA-induced currents via a Gs-protein-coupled pathway. GDP-beta-S in the pipette solution or pretreatment of dorsal root ganglion neurons with pertussis toxin suppressed GABA-induced currents, suggesting that basal Gi/Go-protein activity positively modulates the GABA(A) receptor-channel complex. Mercury chloride potentiation of GABA-activated currents was blocked by application of GTP-gamma-S in the patch pipette or by incubation of neurons with cholera toxin. Mercury chloride potentiation of GABA-activated currents was blocked by application of GDP-beta-S in the patch pipette or by incubation of neurons with pertussis toxin. G proteins, probably Gi/Go proteins, underlie the mercury chloride potentiation of GABA-induced currents.