Pyramidal neurons in the rat CA1 hippocampal area contain both mineralocorticoid (MR) and glucocorticoid receptors (GR) which bind the endogenous adrenal steroid corticosterone with differential affinity. With intracellular electrophysiological recording techniques we have investigated how corticosterone affects the membrane properties of these cells. We observed that low doses (1 nM) of corticosterone or aldosterone can, through MR, reduce the spike frequency accommodation and afterhyperpolarization (AHP) evoked by a short depolarizing current in pyramidal neurons. As the accommodation/AHP can be considered as an intrinsic mechanism of CA1 neurons to attenuate transmission of excitatory input, the MR-mediated action might potentially enhance cellular excitability in the CA1 area. Higher doses of corticosterone or selective glucocorticoids were able to reverse the MR-mediated effect on accommodation/AHP, eventually increasing particularly the amplitude of the AHP. GR-mediated events may thus potentially suppress excitability in the hippocampal CA1 area. Not only current- but also transmitter-induced membrane effects were affected by the steroids. Firstly, GR-ligands were able to suppress a temporary noradrenaline-evoked decrease in accommodation/AHP. Secondly, membrane hyperpolarizations induced by serotonin were reduced by MR-agonists. We propose that cellular excitability in the hippocampus is at least partly under control of coordinative, antagonistic MR- and GR-mediated effects on electrical activity.