Fig. 3
Activation of SK channels by 1-EBIO increased the mAHP amplitude in rats treated with CIE during adolescent stage, which reversed the effects of adolescent CIE on mAHP. a, c Example traces showing action potentials elicited by 200 and 400 pA current injections in NAcS MSNs in the ACSF vs. 1-EBIO (100 μM) from rats treated with CIW (a) or CIE (c) during the adolescent stage. b, d Summarized data showing an increased excitability of NAcS MSNs from rats with a history of CIE (d, ACSF/1-EBIO at 100 μM × Iinj interaction, F7,98 = 2.1, p = 0.04, cell based; F7,21 = 2.5, p = 0.04, animal based) but not CIW (b, ACSF/1-EBIO at 100 μM × Iinj interaction, F7196 = 0.21, p = 0.98, cell based; F7,49 = 0.15, p = 0.99, animal based) during their adolescent stage before vs. during application of 1-EBIO at 100 μM. e Summarized data of maximum spike numbers (Iinj = 400 pA) before and during bath application of 1-EBIO at 100 μM showing a specific increase of excitability in NAcS from rats treated with CIE during their adolescent stage (Ado::CIW/Ado::CIE × ACSF/1-EBIO at 100 μM interaction, F1,21 = 6.9, p = 0.02, cell based; F1,10 = 6.3, p = 0.03, animal based; Bonferroni post test, p < 0.05 between ACSF in Ado::CIE vs. any of the other three groups). f, g Example traces of the first action potential evoked by injecting current at +300 pA in NAcS MSNs from rats with a history of adolescent CIW (f) and CIE (g) before and during 1-EBIO at 100 μM. h, i Summarized results showing increased mAHP amplitude (i, Ado::CIW/Ado::CIE × ACSF/1-EBIO at 100 μM interaction, F1,21 = 4.5, p = 0.04, cell based; F1,10 = 5.0, p = 0.04, animal based; Bonferroni post test, p < 0.05 between ACSF in Ado::CIE vs. either ACSF in Ado::CIW or 1-EBIO at 100 μM in Ado::CIE) but no change in the fAHP (h, Ado::CIW/Ado::CIE × ACSF/1-EBIO at 100 μM interaction, F1,21 = 1.4, p = 0.25, cell based; F1,10 = 1.2, p = 0.30, animal based). j Summarized results showing 1-EBIO at 100 μM increased the normalized mAHP amplitude, by which the decreased mAHP amplitude in rats with an adolescent CIE history was reversed back to that in the CIW control group (Ado::CIW/Ado::CIE × ACSF/1-EBIO at 100 μM interaction, F1,21 = 4.8, p = 0.04, cell based; F1,10 = 5.2, p = 0.04, animal based; Bonferroni post test, p < 0.05 between 1-EBIO at 100 μM in Ado::CIE vs. either ACSF in Ado::CIE or 1-EBIO at 100 μM in Ado::CIW). The cell number/animal number (i.e., m/n) is shown in parentheses for each group. Data were analyzed by two-way ANOVA with repeated measures, followed by Bonferroni post test. *p < 0.05; **p < 0.01
