Protein kinase D promotes plasticity-induced F-actin stabilization in dendritic spines and regulates memory formation.
Bottom Line: In nonneuronal cells, protein kinase D (PKD) has an important role in stabilizing F-actin via multiple molecular pathways.Consequently, impaired PKD functions attenuate activity-dependent changes in hippocampal dendritic spines, including LTP formation, cause morphological alterations in vivo, and have deleterious consequences on spatial memory formation.We thus provide compelling evidence that PKD controls synaptic plasticity and learning by regulating actin stability in dendritic spines.
Affiliation: Department of Physiology and Neurobiology, Eötvös Loránd University, H-1117 Budapest, Hungary.Show MeSH
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Mentions: Previously, we have described a PKD activity reporter, which is suitable to visualize endogenous PKD-mediated phosphorylation events in fixed cells (Fig. 1 A; Czöndör et al., 2009; Fuchs et al., 2009) and is present in the dendritic branches and spines of DIV12-13 hippocampal neurons (see the EGFP signal in Fig. 1 B and Fig. S1 A). To compare the extent of reporter phosphorylation in spines, ratiometric images were created by normalizing the a-pS294 to EGFP signal intensities (Fig. 1 B and Fig. S1 A, ratio images). Only mushroom spines with clearly enlarged heads were chosen for the analysis. To confirm the specificity of the pS294 antibody signal, a mutant reporter construct containing alanine instead of the target serine was also investigated (S/A mutant). In all cases, S/A mutant reporter displayed only a negligible ratio signal (Fig. 1, B–D).
Affiliation: Department of Physiology and Neurobiology, Eötvös Loránd University, H-1117 Budapest, Hungary.