A, perievent histograms of representative SCN multi‐unit responses to electrical stimulation of the OC at varying latencies of GABAergic GHT neuron pre‐stimulation; under control conditions (top), following bath application of the GABAAR antagonist BIC (20 μm; middle), or co‐application of BIC (20 μm) and the GABABR antagonist CGP55845 (3 μm, CGP; bottom). B, normalized mean ± SEM population responses to OC‐stimulation as a function of GHT pre‐stimulation latency (n = 44 GHT‐responsive sites from a total of 81 OC‐responsive sites in three slices). Bath application of BIC substantially attenuated GHT‐driven inhibition at short latencies; residual responses under BIC were further attenuated when co‐applied with CGP. C, normalized mean ± SEM population responses to OC‐stimulation in a separate, second experiment investigating the effects of shorter GHT pre‐stimulation latencies (n = 14 GHT responsive/21 OC‐responsive sites from three slices): note that the initial components of the GHT‐evoked inhibition were almost completely attenuated by BIC application alone. Data in (B) and (C) were analysed by two‐way RM ANOVA with Sidak's post hoc tests (P < 0.01 for GHT pre‐stimulation, treatment and interaction in both cases). Black symbols in (B) and (C) represent significant differences relative to 0 ms delay (***
P < 0.001). Red symbols represent significant differences between BIC and baseline. Blue symbols (B) represent differences between BIC and BIC + CGP (#
P < 0.01, $
P < 0.05).