Figure 6. Thin represses release through dysbindin.

(A) Representative excitatory postsynaptic currents (EPSCs) (individual sweeps and averages are shown in light colors and black, respectively), and mEPSCs (insets) of wild-type (WT) (gray) and presynaptic thin^RNAi (elav^c155-Gal4>UAS-thin^RNAi, ‘+thin^RNAi (pre)’, dark gray), dysb¹ mutants (light red), and presynaptic thin^RNAi in the dysb¹ mutant background (elav^c155-Gal4/Y; UAS-thin^RNAi/+; dysb¹, ‘+thin^RNAi (pre)’, dark red). Mean mEPSC amplitudes (B), EPSC amplitudes (C), and quantal content (D) of the indicated genotypes. Note that presynaptic thin^RNAi expression increases EPSC amplitude and quantal content in WT, but not in dysb¹ mutants. Mean ± standard error of the mean (SEM); WT: n = 17, elav^c155-Gal4>UAS-thin^RNAi: n = 17, dysb¹: n = 12, elav^c155-Gal4/Y; UAS-thin^RNAi/+; dysb¹: n = 12; *p < 0.05; **p < 0.01; ***p < 0.001; n.s.: not significant; two-way analysis of variance (ANOVA) followed by Tukey’s post hoc test. (E) Working model: Our genetic data support a model in which thin controls neurotransmitter release (‘Release’) through negative regulation of dysbindin (‘dysb’).