(A) DopRf02676 mutations suppress LTE induced by AL + NMDA stimulation. Left panel, MB-LexA, LexAop-G-CaMP2/+, one-way ANOVA (F2,18 = 5.932, p<0.001). Right panel, MB-LexA, LexAop-G-CaMP2/+; DopRf02676, one-way ANOVA (F2,18 = 3.479, p=0.053). N = 7 for both genotypes. (B) LTE induced by AL + NMDA stimulation in MB-LexA, LexAop-G-CaMP2 brains is abolished by the addition of the D1R antagonist 10 min prior to AL + NMDA stimulation. Control, F2,15 = 22.148, p<0.001, butaclamol, F2,15 = 0.334, p=0.801, N = 6 for all data. (C) LTE is induced by simultaneous AL + DA stimulation in c309-GAL4; UAS-G-CaMP brains, F2,18 = 5.374, p=0.015, N = 7. (D) LTE can be induced by application of DA alone. One-way ANOVA (F2,18 = 25.306, p<0.001, N = 7). (E) DA-induced LTE in Nmdar1EP331 mutants is indistinguishable from DA-induced LTE in controls. Left panel, MB-LexA, LexAop-G-CaMP2/+, one-way ANOVA (F2,18 = 22.591, p<0.001, N = 7). Right panel, MB-LexA, LexAop-G-CaMP2/+; Nmdar1EP331, one-way ANOVA (F2,15 = 10.335, p=0.002, N = 6). (F) DA-induced LTE is restored in DopRf02676 mutants by expressing a DopR transgene in the MBs. Control (MB-LexA, LexAop-G-CaMP2/+), one-way ANOVA (F2,15 = 8.261, p=0.004). DopRf02676 (MB-LexA, LexAop-G-CaMP2/+; DopRf02676), one-way ANOVA (F2,15 = 0.111, p=0.351). Rescude (MB-LexA, LexAop-G-CaMP2/c747-GAL4; DopRf02676), one-way ANOVA (F2,15 = 5.556, p=0.016). N = 6. (G) LTE induced by DA alone is indistinguishable from LTE induced by AL + DA stimulation. Peak LTE responses plotted as a function of DA concentration. Two-way ANOVA demonstrated significant differences in Ca2+ responses due to DA concentration (F2,30 = 22.49, p<0.0001), but no differences due to the stimulation protocol (DA alone versus DA + AL, F1,30 = 2.869, p=0.1007, N = 6).