Slow clamp currents were recorded from CA1 and CA3 pyramidal neurones in slices of guinea-pig hippocampus maintained in vitro, using a single micro-electrode sample-and-hold technique. Depolarizing voltage commands evoked a time- and voltage-dependent outward current which was suppressed by removing external Ca or by adding Cd (0.5 mM) or Mn (5 mM). This Ca-dependent current (Ic) was not reduced by muscarinic agonists (unlike IM) but was greatly reduced by 5-20 mM-tetraethylammonium (TEA). Repolarizing IC tail currents reversed at -73 +/- 5 mV in 3 mM-K solution. The reversal potential became about 30 mV more positive on raising [K]o to 15 mM. No clear change in current amplitude or tail-current reversal potential occurred on adding Cs (2 mM), reducing [Cl]o from 128 to 10 mM, or replacing external Na with Tris. The underlying conductance GC was activated at membrane potentials positive to -45 mV. At -32 mV GC showed an approximately exponential increase with time, with a time constant of approximately 0.6 sec at 26 degrees C. Repolarizing tail currents declined exponentially with time, the time constant becoming shorter with increasing negative post-pulse potentials. When the clamp was switched off at the end of a depolarizing command of sufficient amplitude and duration to activate IC, a membrane hyperpolarization to -73 mV ensued, of similar amplitude and decay time to that following spontaneous action potentials. It is concluded that the clamp current observed in these experiments is probably the Ca-activated K current thought to contribute to the post-activation after-hyperpolarization in hippocampal neurones.