Figure 6. Elevating cAMP broadly with forskolin revealed localized Ca²⁺ response plasticity in the γ lobe.

(A) Comparison of odor responses before and after pairing of odor with forskolin application, or presenting forskolin alone, in 238Y-GAL4>UAS-GCaMP6f flies (n ≥ 12). *p < 0.05, ***p < 0.001 (Wilcoxon signed-rank test for no odor group, Sidak following ANOVA for all others).

(B) Box plots graphing the change in magnitude of odor responses across different MB regions following pairing of odorant with forskolin (colors) or 1,9-didexyforskolin (gray) in 238Y-GAL4>UAS-GCaMP6f flies (n ≥ 12). Odor responses were significantly elevated following forskolin treatment in the γ lobe at 10, 30, and 100 μM and the heel at 100 μM (# p < 0.05; Wilcoxon signed-rank tests). Forskolin-treated animals showed a significantly larger post / pre odor responses than 1,9-dideoxyfoskolin-treated animals in the γ lobe and heel at 30 μM and 100 μm (*p < 0.05; Mann-Whitney).

(C) Imaging the effects of elevating cAMP in the α, α′, β, and β′ regions with specific drivers (c739-GAL4 for MB α/β neurons and c305a-GAL4 for MB α′/β′ neurons). Box plots are graphed as in panel B. There were no significant differences in post/pre odor response ratios between forskolin and 1,9-dideoxyforskolin groups in any region (Mann-Whitney).

(D) Forskolin (fsk) increased cAMP in both the α tip and γ lobe. The response magnitudes were significantly different (with the α lobe showing larger median increases) between these regions at 10 μM and 30 μM (p < 0.001; Friedman; *p < 0.05; n = 13; Wilcoxon signed-rank), but not 100 μM.