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. 2020 Apr 11;2(1):fcaa043. doi: 10.1093/braincomms/fcaa043

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© The Author(s) (2020). Published by Oxford University Press on behalf of the Guarantors of Brain.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

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Effects of protein kinase and protein phosphatase inhibition on KCl-induced glutamate (Glu) release. Traces of the KCl-induced Glu release after synaptosomal fractions were incubated with or no DMSO (black and grey traces, respectively), R-roscovitine (magenta traces), butyrolactone I (orange traces), SB 216763 (green traces), okadaic acid (ink traces) and cyclosporin A (blue traces) or co-inhibited with R-roscovitive plus okadaic acid (olive traces) and R-roscovitive plus cyclosporin A (teal traces). All traces are the mean ± SD of the measurements in individual animals (n = 4–8 mice per group and gender). Statistical analysis: a two-way ANOVA followed by Bonferroni post hoc comparisons. *P ≤ 0.05, **P ≤ 0.01, ***P ≤ 0.001. B6SJL, mice on the B6SJL background; Cntr, control or vehicle-treated 5XFAD mice, and Tx, EFV-treated 5XFAD mice on the B6SJL background; Cyp46a1^+/+ and Cyp46a1^−/−, wild-type and knockout mice on the C57BL/6J; 129S6/SvEv background.