Pre- and postsynaptic fluxes of Ca2+ and K+ were determined concurrently in CA1 of the hippocampus in vitro under conditions where synaptic transmission was blocked. The Ca2+ entry blocker, Ni2+, abolished both pre- and postsynaptic Ca2+-influx and reduced presynaptic K+-efflux by about 20%. Postsynaptic K+-efflux was reduced nearly by 60%. 4-aminopyridine (4-AP) strongly enhanced presynaptic Ca2+-influx but only marginally increased Ca2+-entry into the postsynaptic neurones. At the same time, total K+-efflux from presynaptic sites was increased by about 30% but was unaltered postsynaptically. Finally, tetraethylammonium (TEA) enhanced both pre- and postsynaptic Ca2+-influx. Postsynaptic influx was more profoundly affected than presynaptic. Neither pre- nor postsynaptic efflux of K+ was altered by TEA. The results indicate a complex balance between inward Ca2+ and outward K+ currents in CA1 and that this balance may differ pre- and postsynaptically.