Fig. 6: Presynaptic cac knockdown abolishes iLN odor responses.
From: Homeostatic synaptic plasticity rescues neural coding reliability
A Experimental scheme. cacRNAi was driven in ORNs using Orco-GAL4. Whole-cell patch clamp recordings were made from iLNs labeled with the 449-QF driver line. B PSTH of the iLN population response to four odors examined as indicated (shaded areas represent SEM, the odor pulse is labeled with a black bar) for 0-day-old flies. Knockdown of cac resulted in an almost complete abolishment of iLN odor responses (final odor dilution of 5 × 10−2; n = 49–50 flies). C PSTH of the iLN population response to four odors examined as indicated (shaded areas represent SEM, the odor pulse is labeled with a black bar) for 2–4-day-old flies. Knockdown of cac resulted in an almost complete loss of iLN odor responses (final odor dilution of 5 × 10−2; n = 49-50 flies). D Quantification of the paired-pulse ratio at different inter-stimulus intervals for 0 day (left) and 2–4-day-old (right) flies (10 ms, 30 ms, 100 ms, 300 ms, and 1000 ms). cacRNAi significantly increased paired-pulse facilitation at short inter-pulse interval [wt day 0, n = 22 (10, 30, 100, and 300 ms), n = 21 (1000 ms); cacRNAi day 0, n = 28 flies. wt day 2–4, n = 13; cacRNAi day 2–4, n = 15 (10 ms), n = 16 flies (30, 100, 300, and 1000 ms)]. Error bars represent SEM. Two-sided two sample t-test, p = 0.002 (10 ms day 0), p = 0.025 (10 ms day 2–4). For all panels **p < 0.01, for detailed statistical analysis, see Table S1.
