Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2018 Jan 18;9:267. doi: 10.1038/s41467-017-02494-0

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© The Author(s) 2018

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/.

PMC Copyright notice

Fig. 6 — Proteasome perturbation increases presynaptic Ca²⁺ influx, RRP size and the amplitude of the fast recovery phase. a Representative two-photon line scans of a control bouton after loading with OGB-1 and Alexa-568. Arrowhead indicates AP-stimulus onset. b Representative spatially averaged Ca²⁺ transients of a control synapse and a DTS^pre synapse (average of 10 sweeps). c Quantification of Ca²⁺-transient peak amplitudes of control and DTS^pre synapses and cumulative frequency plot. Proteasome inhibition results in a significant increase in the peak amplitude compared to control cells. d Baseline fluorescence of the Ca²⁺ indicator OGB-1 and the Ca²⁺-independent dye Alexa-568 in the two genotypes. Baseline OGB-1 fluorescence is significantly higher in DTS^pre synapses. The decay time constant τ is not changed. Mean ± s.e.m.; n ≥ 53 boutons; *p < 0.05; ****p < 0.00001; Wilcoxon rank-sum test. e Left: Representative EPSC trains in response to 60-Hz stimulation (60 stimuli, 1 mM [Ca²⁺]_e) for control cells and DTS^pre mutant cells. Right: cumulative EPSC charge was calculated by back-extrapolation of a linear fit (black line) to the last 15 stimuli of the cumulative EPSC integrals to time point zero. f RRP size was calculated by dividing cumulative EPSC charge by the average mEPSC charge. g Left: Example of EPSCs during 60-Hz stimulation (60 stimuli, 2 mM [Ca²⁺]_e) followed by recovery pulses given at intervals of 25, 75, 175 and 475 ms after the last train stimulus of the indicated genotypes. Right: Average recovery (mean EPSC amplitude at a given interval divided by the first EPSC amplitude of the 60 Hz train) versus recovery interval (Δt) of the indicated genotypes superimposed with biexponential fits. Inset shows the data at short intervals. Biexponential fits of average data gave the time constants noted in the figure. h Average amplitude of the fast recovery component ‘A_fast’ of the two groups obtained from bi-exponential fits of individual synapses. Note the significant increase in the fast recovery component in DTS^pre mutants (there was no difference in A_slow and recovery kinetics between the two groups). Mean ± s.e.m.; n ≥ 10 cells; *p < 0.05; **p < 0.001; Student’s t-test