Opponent effects of potassium on GABAA-mediated postsynaptic inhibition in the rat hippocampus.

1. The effects of raising the concentration of extracellular potassium ([K+]o) on gamma aminobutyric acid (GABA)-mediated inhibitory postsynaptic potentials (IPSPs) were investigated in adult rat hippocampal slices using intracellular recording techniques. IPSPs were evoked in CA1 pyramidal neurons by direct activation of inhibitory interneurons in slices treated with glutamatergic antagonists to block excitatory synaptic transmission. The fast (Cl(-)-dependent, GABAA receptor-mediated) IPSPs (fIPSPs) were isolated from the slow (K(+)-dependent; GABAB receptor-mediated) IPSPs (sIPSPs) by intracellular injection of QX-314, which also suppressed fast (Na(+)-dependent) action potentials. 2. In normal (3.5 mM) and in high (7.5 mM) [K+]o, the peak fIPSP amplitude changed nonlinearly with membrane potential (VM) in a way consistent with outward rectification of the underlying conductance. The input conductance of the fIPSP (GfIPSP) measured around resting VM (about -67 mV) increased 1.7-fold on changing from normal to high-K+ saline, whereas resting VM depolarized 6.8 mV. Repolarizing VM reversed the increase in GfIPSP, suggesting that it was due to outward rectification. The resting input conductance of the neurons increased 1.4-fold in high K+. 3. The time course of fIPSPs was prolonged by high K+. The half time of fIPSP decay increased 1.4-fold, and in half of the neurons the decay became conspicuously multipeaked, suggesting that neurally evoked GABA release from inhibitory interneurons was prolonged. 4. In normal K+, the reversal potentials of fIPSPs (EfIPSP; -76.5 mV) was 9.7 mV more negative than resting VM. Polarizing VM 10-20 mV for 15 min with current injection did not change EfIPSP appreciably.(ABSTRACT TRUNCATED AT 250 WORDS)