Fig 1: MK801-induced synaptic plasticity deficit in the DG can be reversed by isoflurane treatment. (A–C) Representative Western blotting images of proteins (A) and densitometric quantification (B,C) for NR2A and NR2B in the DG. a-tubulin was used as the loading control (n = 3 mice per group. One-way ANOVA, F(2, 9) = 9.306, p = 0.062; post hoc test: Ctrl vs. MK801, p = 0.73; MK801 vs. MK801+ISO, p = 0.92; Ctrl vs. MK801+ISO, p = 0.83 shown on B; One-way ANOVA, F(2, 9) = 1.588, p = 0.256; post hoc test: Ctrl vs. MK801, p = 0.16; MK801 vs. MK801+ISO, p = 0.48; Ctrl vs. MK801+ISO, p = 0.31 shown on (C)). (D) Electrode configuration for the LTP recording in the DG. The red rectangle indicates the stimulating electrode (left) and recording electrode (right). Scale bar, 100 µm. (E) LTP of local field potential in the DG after HFS induction at the perforant path. LTP was enhanced in the DG by isoflurane treatment after MK801 injection (n = 5 mice per group). (F) Quantitative analysis of data in (E). (Two-way ANOVA, F(2, 1260) = 713.5, p < 0.0001; post hoc test: Ctrl vs. MK801, p < 0.0001; MK801 vs. MK801+ISO, p < 0.0001; Ctrl vs. MK801+ISO, p < 0.05). Data are represented as mean ± SEM, * p < 0.05, **** p < 0.0001, ns, not significant.