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: 16 h of KCl-induced depolarization significantly increased the ratio of mushroom spines (Fig. 3, A and C) without affecting spine density (not depicted). KCl-induced changes in spine morphology were also evident when individual spines were plotted according to their length and HN index (head/neck width ratio; Fig. 3 B). As this happened at the expense of thin, filamentous spines, we assume that long-term depolarization leads to F-actin stabilization and, consequently, the expansion of dendritic spine heads. Collectively, our data indicate decreased actin dynamics when enlarged dendritic spine heads are already stabilized.
Affiliation: Department of Physiology and Neurobiology, Eötvös Loránd University, H-1117 Budapest, Hungary.