Fig. 3
NMDAR dysfunction in lateral amygdala of St8sia2−/− mice. a–f AMPA- and NMDA currents were recorded in pyramidal neurons in the lateral amygdala (LA) at cortical (left column) and subcortical (right column) inputs. a, b Wide-field images and diagrams indicate typical positioning of the bipolar electrode for stimulation of cortical (a) and subcortical (b) afferents. Representative synaptic currents evoked at − 70 mV (AMPA) and + 40 mV after AMPAR blockade (NMDA) are shown for wild-type (WT, black) and St8sia2−/− (KO, blue) mice. c At cortical inputs, AMPA/NMDA ratio was measured during early postnatal stage (1–2 weeks: unpaired t-test, t24 = 2.31, p = 0.029), juvenile period (4–5 weeks: Mann–Whitney test, U = 18, p = 0.0076), young adults (8–11 weeks, t13 = 2.41, p = 0.031) and in older mice (11–18 weeks: t18 = 3.67, p = 0.0017). d Same measurements as in c for subcortical inputs (p > 0.05 at all developmental stages). e, f Input–output curves of NMDA currents (top) and AMPAR currents (bottom) elicited at cortical (e) and subcortical (f) inputs with increasing stimulus intensities, revealing decreased NMDAR-mediated output at cortical synapses from St8sia2−/− mice (two-way ANOVA: main effect of genotype: F1,14 = 5.97, p = 0.0284). Color-coded traces are representative mean currents (average of four traces) elicited at the different intensities. g, h Effect of GluN2B-specific antagonist CP-101,606 (10 µM) on cortically (g) and subcortically (h) evoked NMDAR currents in WT and St8sia2−/− mice (unpaired t-test for mean values in the shaded area, t13 = 3.28, p = 0.006 for g, and t14 = 3.006, p = 0.0094 for h). Traces at the top are NMDAR currents during baseline, after superfusion of CP-101,606 (magenta) and of the NMDAR blocker D,L-APV (100 µM), which abolished the residual current (gray). Results are given as mean ± SEM. *p < 0.05; **p < 0.01
