Effects of kainate on the excitability of rat hippocampal neurones

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.