Fig. 5: ZDHHC8 regulates postsynaptic AMPA receptor function in the Mg²⁺-free model in vitro.

a Representative traces showing evoked AMPARs (bottom; holding at −70 mV) and NMDAR EPSCs (top; holding at +40 mV) recorded from CA1 pyramidal cells in hippocampal slices. b Bar graphs showing the ratio of AMPAR/NMDAR EPSCs (n = 4 mice per group; *P < 0.05, ***P < 0.01). c, d Summary of the effects of ZDHHC8 on absolute peak current amplitudes mediated by AMPARs or NMDARs. NMDAR-mediated responses were measured at 50 ms post-stimulus (the numbers of cells in b, *P < 0.05, ***P < 0.001; N.S. represents no significance). e Representative sample traces of paired-pulse facilitation measurements obtained with a 50-ms inter-stimulus. f Bar graphs showing the PPR (n = 4 mice per group; P > 0.05). g–i Current–voltage (I–V) relationships were derived for AMPAR-mediated currents from CA1 pyramidal cells. g Representative traces of AMPA currents were recorded at various holding potentials (−60, −40, −20, 0, +20, +40, and +60 mV). h I–V curves of AMPA currents. All AMPAR EPSC values were normalized at −60 mV as a function of holding potential (mV), showing the inward rectification at positive holding potentials in ordinate. i Bar plot of the rectification index (RI) (RI was calculated as the AMPAR-mediated current response at −60 mV/+40 mV; n = 4 mice per group; *P < 0.05, ***P < 0.001; one-way ANOVA). j, k Representative traces (j) and bar plot (k) of AMPAR/NMDAR EPSCs (top) before and after IEM-1460 (50 µM) application (bottom). The data represent the mean ± SEM (*P < 0.05; two-way ANOVA with Bonferroni’s post hoc test)