Fig. 3.
The synaptoneurosomal GluA1 subunit of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) was increased, after the administration of isoflurane. (A) Experimental design. Synaptoneurosomes and whole lysates of GluA1, one of the subunits of AMPAR, of the dorsal hippocampus were measured 1, 7, and 28 days after a 2-h exposure to 1.8% isoflurane (Iso). Comparisons were made between the control and isoflurane groups. (B) The amount of synaptoneurosomal GluA1 was significantly increased on day 7 (day 1, n = 5 or 6; day 7, n = 7 or 8; day 28, n = 5 or 6; isoflurane, F[1, 27] = 6.933, *P = 0.014; day, F[2, 27] = 0.783, P = 0.783; isoflurane × day, F[2, 27] = 0.783, P = 0.783; *P =0.012 at day 7 control vs. isoflurane). (C) The amount of GluA1 in the whole lysates was not significantly changed (day 1, n = 5 or 6; day 7, n = 7 or 8; day 28, n = 5 or 6; isoflurane, F[1, 30] = 0.620, P = 0.437; day, F[2, 30] = 2.279, P = 0.120; isoflurane × day, F[2, 30] = 2.279, P = 0.120). GluA1 was normalized to the levels of β-actin (BA). All statistical analyses were performed using two-way factorial ANOVA (isoflurane × day, significance level was set at P < 0.05) followed by Student t tests (significance level was set at 0.05/3 = 0.0167 with Bonferroni correction). Data are shown as mean ± SEM. ns = absence of significant differences.