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Fig. 3. Involvement of SK channels in the Zn2+-mediated augmentation of excitability in SNc dopaminergic neurons. (A) Current-injected voltage raw traces by a depolarizing pulse (100 pA current injection for 1 s). Top, 100 nM Apamin; Bottom, 10 μM Paxilline. (B) Spike frequency changes by inhibition of SK channels but not by BK channels (100 nM Apamin, 1.97±0.29, n=4; 100 nM Iberiotoxin, 1.00±0.10, n=4; 10 μM Paxilline, 1.00±0.0, n=4; #p<0.05, one sample t-test, hypothetical value=1). (C) Significant decrease in Zn2+-induced augmentation of activity by apamin (100 μM Zn: Control, 1.81±0.15, n=13; Apamin, 0.98±0.13, n=4; Iberiotoxin, 1.86±0.38, n=4; Paxilline, 1.65±0.16, n=4; p<0.05, one-way ANOVA; Wash: Control, 1.43±0.2, n=12; Apamin, 0.64±0.25, n=4; Iberiotoxin, 1.24±0.12, n=4; Paxilline, 1.53±0.15, n=4; p>0.05, one-way ANOVA; *p<0.05; Dunnett’s post-hoc multiple comparison test for control).
Exp Neurobiol 2019;28:578~592
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