Intracellular recordings from CA1 pyramidal neurones of the rat hippocampal slice preparation were used to study changes in neuronal excitability induced by the excitatory amino acid analogues kainate (KA) and N-methyl-D-aspartate (NMDA). Low concentrations of bath-applied KA (50-200 nM) or NMDA (1-3 microM) elicited a relatively small membrane depolarization and increased the number of spikes fired by a constant current pulse. The spike after-hyperpolarization (AHP) was depressed by KA but enhanced by NMDA. After blockade of the voltage-sensitive Na+ conductances with tetrodotoxin, intracellularly applied current pulses elicited Ca2+ spikes. Whereas NMDA always increased the duration (and number) of Ca2+ spikes and of their AHP, KA conversely reduced these spikes and (in almost half of the cells tested) the late phase of their AHP. When Ba2+ was used to replace extracellular Ca2+, prolonged plateau potentials developed and were also blocked by KA. NMDA had no effect on Ba2(+)-dependent responses. These results suggest that low concentrations of KA profoundly modified the electroresponsiveness of CA1 neurones perhaps by depressing a Ca2(+)-dependent K+ conductance mechanism responsible for dampening the excitability of these cells.