Fig. 5.

(R,S)-ketamine and prucalopride exhibit a common mechanism by reducing large AMPA-driven synaptic bursts in CA3. a Experimental design. b The average EPSC amplitude did not differ between the groups. c The average number of EPSCs (within a 20-s recording window) did not differ between the groups. d Saline-treated mice typically displayed large bursts of EPSCs (−590.8 ± 13.85 pA), which were blocked by the AMPA receptor antagonist NBQX. These large AMPA receptor-mediated signals were not present in either e (R,S)-ketamine- or f prucalopride-treated mice. (n = 5–7 mice per group). Error bars represent ± SEM. Sal saline, K (R,S)-ketamine, Prucal prucalopride, CA3 Cornu Ammonis 3, pA picoamps, EPSCs excitatory postsynaptic currents, no. number, NBQX 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo[f]quinoxaline, mg milligram, kg kilogram, ms millisecond