Fig. 5
Glutamate receptor perturbation and proteasome perturbation enhance release of EGTA-sensitive vesicles. a Representative EPSC traces of control (elavC155,’ctrl’) and DTSpre (elavC155-Gal4;UAS-DTS5; ‘DTSpre’) synapses. The two left EPSC traces from each genotype were recorded from synapses treated with 50 µM EGTA-AM for 10 min or DMSO as control. The last two EPSC traces were recorded from synapses treated with 30 µM PhTX for 10 min, followed by wash and treatment with 50 µM EGTA-AM or DMSO for 10 min (1 mM [Ca2+]e). The red bars symbolize that the decrease after PhTX and EGTA application compared to untreated cells is similar in both genotypes. b Quantification of EPSC amplitude and EPSC charge of the experiment shown in (a). EGTA-AM application induces a significant decrease in EPSC charge in DTSpre mutants, whereas there is no significant decrease in EPSC charge at control synapses. After PhTX and EGTA treatment, EPSC amplitudes are significantly smaller in controls than in DTSpre mutants (p = 0.0197; unpaired t-test). By contrast, there is no significant difference between both groups in the absence of EGTA treatment (p = 0.7), indicating that controls are more EGTA sensitive during homeostatic plasticity than DTSpre mutants. The increased EGTA-AM sensitivity after PhTX incubation implies that the induction of PHP requires increased recruitment of EGTA-sensitive, low-p r vesicles. Mean ± s.e.m.; n ≥ 10 cells; *p < 0.05; **p < 0.001; ****p < 0.00001; ANOVA and Tukey’s multiple comparison tests
