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. 2020 Feb 4;10:1777. doi: 10.1038/s41598-020-58610-6

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© The Author(s) 2020

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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PKCα regulates Rac1 activation during sLTP via PDZ binding domain. (a) Primary structure of PKCα showing pseudosubstrate, C1A and C1B domains, C2 domain, kinase domain, C-terminal tail, and PDZ binding motif. (b,c) Time courses and quantification of transient (1–3 min) and sustained (10–25 min) spine volume change (b) and transient and sustained Rac1 activation (c) induced by glutamate uncaging in PKCα KO hippocampal neurons expressing PKCα or PKCα without PDZ domain (PKCα-no PDZ). n = 20/22 PKCα and 14/18 PKCα-no PDZ (neurons/spines). Data are mean ± s.e.m. *P < 0.05, two-tailed t-test. (d) Schematic of potential PKCα regulation of Rac1.