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. 2017 Nov 9;8:1380. doi: 10.1038/s41467-017-01704-z

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 6 — AIPR-1 inhibits synchrony of spontaneous release. a Mutation of unc-64 (syntaxin) precluded the enhancing effect of aipr-1(zw86) on the amplitude of spontaneous miniature currents (minis). Frequency, mean amplitude, and amplitude distribution of minis are compared among the wild type (wt) (n = 9), aipr-1(zw86) (n = 7), unc-64(e246) (n = 9), and aipr-1(zw86) unc-64(e246) (n = 8). It is noteworthy that the aipr-1 mutation increased large-amplitude events in the amplitude distribution graph and this effect was eliminated by a mutation in unc-64. b Comparison of 10–90% rise time of minis between wild type (wt) and aipr-1(zw86). The sample minis were normalized in amplitude and superimposed at an identical time scale. Data are shown as mean ± SEM. *p < 0.05, ***p < 0.001 compared with wt; ^# p < 0.05, ^### p < 0.001, and NS (p > 0.05) compared between indicated groups (one-way ANOVA followed by Tukey’s post-hoc test)