Effects of NO deprivation on the development of SLEs in hippocampal–entorhinal cortex slices from mice. A, Comparison of the effects of different NOS inhibitors on the development of SLEs. Under low-Mg²⁺ condition, the onset latency of SLEs was 35 ± 4 min (n = 24) in untreated hippocampal–entorhinal cortex slices, as indicated by the appearance of transient increase in [K⁺]_o (top trace). NO deprivation by l-NMMA/PTIO prevented development of SLEs. Similarly to l-NMMA, the nNOS inhibitor 7-NI (middle traces) but not the iNOS inhibitor aminoguanidine (AG) (bottom trace) prevented the development of SLEs in combination with PTIO. The effects were reversible after washout of the NOS inhibitors and PTIO. B, Application of l-NMMA/PTIO prevented the development of SLEs specifically by NO deprivation, because application of the NO donor SNAP initiated SLEs despite the presence of l-NMMA/PTIO. C, Diagram summarizing the SLE onset latencies in control and NO-deprived hippocampal–entorhinal cortex slices. The last column represents the group, in which SNAP was applied in the presence of l-NMMA/PTIO after 1 h of NO deprivation under low-Mg²⁺ condition.