Figure 5.

cAMP elevation in dfmr1³/+ reverses their learning deficit. Mean PIs and their SEMs (PI ± SEM) are shown for all experiments. Where appropriate, animals were heterozygous for all transgenes, Gal4 drivers, and Gal80^ts. A, Rolipram administration (open circles) resulted in performance indistinguishable from that of controls (filled diamonds) after two, four, and six pairing training (p = 0.16, p = 0.04, and p = 0.73, respectively). The performance of untreated animals (open squares) remained significantly different from both (p < 0.001). n ≥ 8. B, Rolipram administration (gray bar) to animals with pan-neuronally abrogated dfmr1 resulted in learning equivalent to that of control driver heterozygotes (p = 0.44) or UAS-dfmr1-R heterozygotes (p = 0.98). The performance of untreated animals (open bars) remained significantly different from all other groups (p < 0.0001). n ≥ 10. C, Genetic rescue of the dfmr1³/+ learning deficit by reduction of functional DNC. The performances of dnc¹/+; dfmr1³/+ double heterozygotes and dnc^ML/+; dfmr1³/+ (gray bars) are not statistically distinguishable (p = 0.15 and p = 0.36, respectively) from that of w¹¹¹⁸ controls (black bar). In contrast, the performances of dnc¹ heterozygotes and dfmr1³/+ (open bars) were significantly different from controls (p < 0.0001 for both). n ≥ 8.