Interaction of lithium with postsynaptic inhibition in guinea pig hippocampal neurons

Intracellular recording techniques were used to study the effects of Li+ on postsynaptic inhibition of CA3 neurons in guinea pig hippocampal slices. Carbachol (0.3 microM) suppressed and phenylephrine (3 microM) enhanced the hyperpolarization induced by baclofen (0.15 microM). Low intracellular concentrations of Li+ (less than 10 microM) suppressed the muscarinic blockade of the K(+)-dependent inhibition, leaving its enhancement by noradrenergic receptor stimulation unchanged. K(+)-dependent inhibition per se was not affected. At high intracellular concentrations Li+ impaired postsynaptic Cl(-)-dependent inhibition by reducing the efficacy of an outward Cl- pump. While the effect of Li+ on the modulation of K(+)-dependent inhibition may be therapeutically relevant, its action on Cl(-)-dependent inhibition may underly some toxic effects.