Fig. 4
Blockade of SK channels by apamin decreased the mAHP amplitude in rats treated with CIW during the adolescent stage, which mimicked 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. apamin (300 nM) from rats treated with CIW (a) and CIE (c) during the adolescent stage. b, d Summarized data showing an increased excitability of NAcS MSNs from rats with a history of CIW (b, ACSF/apamin at 300 nM × Iinj interaction, F7238 = 2.6, p = 0.01, cell based; F7,35 = 2.3, p = 0.04, animal based) but not CIE (d, ACSF/apamin at 300 nM × Iin interaction F7126 = 0.3, p = 0.97, cell based; F7,28 = 0.4, p = 0.89, animal based) during their adolescent stage. e Summarized data of spike number (Iinj = 400 pA) before and during bath application of apamin (300 nM) showing a specific increase of excitability in NAcS from rats treated with CIW during their adolescent stage (Ado::CIW/Ado::CIE × ACSF/apamin at 300 nM interaction, F1,26 = 6.9, p = 0.01, cell based; F1,9 = 6.2, p = 0.03, animal based; Bonferroni post test, p < 0.05 between ACSF in Ado::CIW vs. either apamin at 300 nM in Ado::CIW or ACSF in Ado::CIE). f, g Example traces of the first action potential evoked at Iinj = 300 pA in NAcS MSNs from rats with a history of adolescent CIW (f) and CIE (g) before and during apamin at 300 nM. h, i Summarized results showing apamin at 300 nM increased mAHP amplitude (i, Ado::CIW/Ado::CIE × ACSF/apamin at 300 nM interaction, F1,26 = 6.3, p = 0.02, cell based; F1,9 = 5.8, p = 0.04, animal based; Bonferroni post test, p < 0.05 between ACSF in Ado::CIW vs. either ACSF in Ado::CIE or apamin at 300 nM in Ado::CIW) but no significant effects were detected on the fAHP amplitude (h, Ado::CIW/Ado::CIE × ACSF/apamin at 300 nM interaction, F1,26 = 0.1, p = 0.83, cell based; F1,9 = 0.2, p = 0.67, animal based) in adolescent CIE- vs. CIW rats. j Summarized results showing apamin at 300 nM decreased the mAHP amplitude in adolescent CIW rats (Ado::CIW/Ado::CIE × ACSF/apamin at 300 nM interaction, F1,26 = 5.7, p = 0.02, cell based; F1,9 = 5.6, p = 0.04, animal based; Bonferroni post test, p < 0.05 between apamin at 300 nM in Ado::CIW vs. either ACSF in Ado::CIW or apamin at 300 nM in Ado::CIE). It is observed that the adolescent CIE effects on the amplitude of mAHP were mimicked in the CIW control group. 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
