Figure 7. Suppression of axonal DA release by SUR1-based KATP-channels does not occur via decreased cholinergic tone at nAChRs.
A and B. Representative 1 p and 5 p evoked [DA]o recorded in striatal slices in the absence (black traces) and presence (red traces) of mecamylamine (500 nM), a nAChR antagonist (A) or diazoxide (60 μM), a SUR1-selective KATP-channel opener (B). C. Mean data for the effect of mecamylamine on peak [DA]o evoked by 1 p or 5 p (Mec, n = 9 recording sites) showing suppression of [DA]o evoked by 1 p and 5 p at 10 Hz, maintenance of release with 5 p at 25 Hz, and enhancement of peak [DA]o evoked with 5 p at 100 Hz (**p < 0.01, ***p < 0.001 vs. control; two-way ANOVA with Bonferroni's post-hoc analysis). Consequently, in mecamylamine peak [DA]o evoked by 5 p at ≥ 25 Hz was significantly higher than that evoked by 1 p (###p < 0.001 vs. respective 1 p evoked [DA]o,; one-way ANOVA with Dunnett's multiple comparisons). D. Ratio of 5 p to 1 p evoked [DA]o showing an enhanced frequency-dependence in the presence of mecamylamine (n = 9 recording sites; **p < 0.01; ***p < 0.001 vs. control, twoway ANOVA with Bonferroni's post-hoc analysis; ###p < 0.001 vs. respective 10 Hz evoked [DA]o; one-way ANOVA with Dunnett's multiple comparisons). E. Mean data for the effect of diazoxide on peak [DA]o evoked by 1 p or 5 p (n = 9 recording sites) showing a similar suppression of peak [DA]o evoked by 1 p and 5 p at all stimulation frequencies (*p < 0.05;**p < 0.01 vs. control; two-way ANOVA with Bonferroni's post-hoc analysis). F. Ratio of 5 p to 1 p evoked [DA]o across frequencies was unaltered by diaxoxide (n = 9 recording sites; p > 0.05 vs. control at all frequencies; two-way ANOVA with Bonferroni's post-hoc analysis).