Fig. 2.
Fmr1 KO mice reduced KARs-mediated EPSCs in pyramidal neurons of layer II/III insular cortex. a, b, To detect KARs-mediated EPSCs, AMPAR/KAR mediated EPSCs were obtained in the presence of GABAA receptor antagonist, PTX (100 μM) and a NMDARs angatonist, AP-5 (50 μM) for 5 min in Fmr1 WT (Aa) and KO mice (Ba). 10 min after the perfusion of an AMPAR antagonist, GYKI 53655 (100 μM), a residual current remained (A-Bb). The small currents could be totally blocked by a AMPAR/KARs antagonist, CNQX (20 μM) in Fmr1 WT (Ac) and Fmr1 KO mice (Bc). c, Statistical results of the percentage of EPSCs in the presence of GYKI 53655 (n = 15 in 11 Fmr1 WT mice, n = 13 in 9 Fmr1 KO mice), and CNQX (n = 6 in 6 Fmr1 WT mice, n = 5 in 4 Fmr1 KO mice). Compared with KARs mediated currents in Fmr1 WT mice, KAR-mediated currents in Fmr1 KO mice were significantly decreased (*P < 0.05). d, KA receptor-mediated EPSCs show slower kinetics in Fmr1 WT and Fmr1 KO mice. Normalized traces of GYKI53655-sensitive and GYKI53655-resistant EPSCs were recorded. e, The data of averaged rise time and decay time in GYKI-sensitive and GYKI-resistant traces. The rise time in GYKI53655-resistant EPSCs between Fmr1 WT and Fmr1 KO mice were significantly different (n = 13 in 10 Fmr1 WT mice, n = 12 in 10 Fmr1 KO mice) (*P < 0.05)