The purpose of this research was to estimate the usefulness of sodium nitroprusside (SNP) as a donor of nitric oxide (NO) in the study of synaptic plasticity. The influence of SNP, K3Fe(CN)6 and K4Fe(CN)6 on the evoked potential recorded from mouse hippocampal slices was evaluated. When slices were exposed to 1 mM SNP for no longer than 15 min, a facilitation of the population spike was observed following perfusion. Longer, 60 min exposure of the slices to 1 mM SNP prevented this perfusion-induced amplification of the potential and blocked the induction of LTP by subsequently applied high frequency stimulation (HFS). SNP at lower concentrations (0.2 mM) had no effect. SNP (1 mM) suppressed the NMDA component of the population spike. Light inactivated, 1.0 mM SNP, when applied for 15 min, reduced the potential and subsequently induced LTP. However, longer exposure of the slices to the light inactivated 1 mM SNP made the potential unstable and blocked induction of LTP. K3Fe(CN)6 and K4Fe(CN)6, molecules structurally related to SNP but unable to generate NO, transiently amplified the population spike and its NMDA component. We suggest that SNP, which is often used as nitric oxide donor, exerts a dual inhibitory and facilitatory action on hippocampal evoked potentials. The possible mechanisms of these actions are discussed.