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. 2011 Nov 2;108(46):18831–18836. doi: 10.1073/pnas.1114569108

Fig. 2.

Fig. 2.

Tissue-specific regulation of changes in different neurotransmitter systems and behaviors. (A) EJC amplitude was reduced significantly by expression of the Ddysb RNAi presynaptically (elav-Gal4/Y; DdysbIR-1/+) but not postsynaptically (DdysbIR-1/+;C57/+) (ANOVA; n = 9–16). The calcium concentration for recording is 0.4 mM. (B) Neuronal expression of UAS-Ddysb (elav-Gal4/Y;UAS-Ddysb/+;dysb1) rescued the EJC deficit in the dysb1 mutant (ANOVA; n = 16–22). (C) Glial expression of Ddysb (UAS-Ddysb/+;Repo-Gal4 dysb1/dysb1), but not neuronal expression of Ddysb (UAS-Ddysb/+;elav-Gal4(III) dysb1/dysb1), restored the brain dopamine concentration to normal levels (ANOVA; n = 5–10). (D) Pan-neural expression of Ddysb (UAS-Ddysb/+;elav-Gal4(III) dysb1/dysb1) is sufficient to rescue the 3-min associative memory deficit in the dysb1 mutant. However, glia-specific expression of Ddysb (UAS-Ddysb/+;Repo-Gal4 dysb1/dysb1) failed to do so (ANOVA; n = 4–14). (E and F) Locomotor hyperactivity and mating disorientation were suppressed in dysb1 mutants expressing UAS-Ddysb in glia (UAS-Ddysb/+;Repo-Gal4 dysb1/dysb1) but not in neurons (UAS-Ddysb/+;elav-Gal4(III) dysb1/dysb1). (ANOVA; n = 8–10 for locomotor test; n = 22–51 for mating test.) Data are means ± SEM. (G and I) Pan-neuronal expression of Hdysb rescued the EJC amplitude (elav-Gal4/Y;UAS-Hdysb/+;dysb1) (ANOVA; n = 9–10) and the 3-min associative memory deficit (UAS-Hdysb/+;elav-Gal4(III) dysb1/dysb1) (ANOVA; n = 16) in the dysb1 mutant. Calcium concentration for recording is 0.4 mM. (H and J) Glial expression of Hdysb (UAS-Hdysb/+;Repo-Gal4 dysb1/dysb1) restored the brain dopamine level (ANOVA; n = 4–11) and partially suppressed the hyperactivity in the dysb1 mutant (ANOVA; n = 10). Data are means ± SEM. *P < 0.05; **P < 0.01; ***P < 0.001; n.s., not significant (P > 0.05).