Fig. 5

Enhanced presynaptic glutamate release within aIC after TNBS treatment. a: Representative sEPSCs recorded in the superficial layer of aIC from sham (top) and TNBS-treated (bottom) rats holding at − 60 mV. b: Cumulative inter-event interval (left) and amplitude (right) histograms of sEPSCs recorded in the same neurons showed in (a). c: Summary plots showing the frequency (left) and the amplitude (right) of sEPSC was increased in CP rats (1.46 ± 0.28 Hz, 18.48 ± 0.84 pA, n = 12) compared to sham rats (0.65 ± 0.26 Hz, 15.06 ± 0.96 pA, n = 11), unpaired t-test. d: Representative traces of PPF with an interval of 35 ms recorded in the superficial layer of aIC (top). PPF at time intervals of 35, 50 and 75 ms was reduced in CP rats (bottom). n = 13 cells in sham group and 15 in TNBS group, one-way repeated ANOVA. e: Representative western blot sample for VGluT1 within aIC obtained on POD 7, 14 and 28 (top). Statistical analyses showing enhanced expression of VGluT1 from POD 7 to 28 after TNBS treatment (bottom). n = 3 rats in each group, one-way ANOVA. f: The immunoreactivities of VGluT1 within aIC were remarkably increased in TNBS-treated rats compared to sham rats. Microphotographs indicating double-immunoflurescence histochemistry for VGluT1 (green) and NeuN (red) within aIC (left). The framed areas in upper images were magnified in lower images. Bars = 200 μm in upper images and 40 μm in lower images. Quantifications and statistical analyses of VGluT1 immunoreactivities presented in the graph (right). * P < 0.05, ** P < 0.01, TNBS vs sham