Somatodendritic release was characterized in substantia nigra dopamine neurons. Release was induced using a monopolar electrode and measured by recording D2 receptor IPSCs in control mice (RIM control) and in mice with conditional knockout of RIM specifically in dopamine neurons (RIM cKODA). (A, B) Example traces (A) and quantification (B) of IPSCs in RIM control and RIM cKODA mice with vs. without the presence of the D2 receptor antagonist sulpiride, n = 23 cells/6 mice in RIM control, and n = 23/6 in RIM cKODA, significance was calculated by two-way ANOVA and is reported in panel B (RIM control vs. RIM cKODA: F(1) = 57.63, p < 0.001; stimulated response vs. + sulpiride: F(1) = 60.71, p < 0.001), and was followed by Bonferroni post-hoc analysis (RIM control stimulated response vs. RIM control + sulpiride t = 9.70, p < 0.05; RIM cKODA stimulated response vs. RIM cKODA + sulpiride: t = 1.33, p > 0.05; RIM control stimulated response vs. RIM cKODA stimulated response: t = 9.62, p < 0.05). (C, D) Example traces (top) and quantification (bottom) of IPSCs stimulated in RIM control slices (C) or RIM cKODA slices (D) before and after treatment with L-DOPA (10 µM) and subsequent application of sumatriptan (1 µM, to inhibit dopamine release from serotonin terminals), n = 6 cells/6 mice in each group, significance was calculated by repeated measures ANOVA and is reported in panels C and D, (C: F = 10.44, p = 0.01 D: F = 22.75, p < 0.005), and was followed by Tukey’s multiple comparison test (C: baseline vs. L-DOPA p < 0.05, L-DOPA vs. sumatriptan p < 0.05; D: baseline vs. L-DOPA p < 0.05, L-DOPA vs. sumatriptan p < 0.05). Data in B-D are shown as mean ± standard error of mean (SEM) and small circles represent individual cells.