Fig. 3
Extent of inhibitory action of NMDA receptor-mediated currents by activation of 5-HT1A receptors did not affect L5 pyramidal neurons in the 15q dup mouse model. a Representative time course of reversible reduction of NMDA-EPSCs by bath-application of the 5-HT1A receptor agonist 8-OH-DPAT (20 μM for 5 min, trace ii). At the end of the recording, EPSC amplitude was completely suppressed by the NMDAR antagonist APV (50 μM, trace iii), indicating that the recorded synaptic current was mediated by the NMDARs. Right traces were obtained at the time points indicated in the graph of the left. Trace i indicates the baseline level of NMDA-EPSC. These recordings were conducted in the presence of gabazine (500 nM) and CNQX (10 μM) in order to block both GABAA- and AMPA/kainate-receptor mediated synaptic transmissions. b Effects of bath-application of 8-OH-DPAT on NMDA-EPSC amplitude at a holding potential of + 50 mV. The amplitude of NMDA-EPSCs was expressed as a percentage of the baseline (determined for 10 min before application of 8-OH-DPAT). The inhibitory action on NMDA-EPSCs by 8-OH-DPAT was similar in both genotypes at 5–7 min (WT (open circles): 71.36 ± 2.96%, n = 12; 15q dup (filled circles): 75.75 ± 3.90% n = 14, t (24) = − 0.87, p = 0.39; unpaired t-test). Each symbol represents mean ± S.E.M. Right traces were shown as representative recordings. The traces shown are the average of eight consecutive sweeps recorded at the time points indicated in the time course of the left graph