Protein kinase D promotes plasticity-induced F-actin stabilization in dendritic spines and regulates memory formation.

Abstract

Actin turnover in dendritic spines influences spine development, morphology, and plasticity, with functional consequences on learning and memory formation. In nonneuronal cells, protein kinase D (PKD) has an important role in stabilizing F-actin via multiple molecular pathways. Using in vitro models of neuronal plasticity, such as glycine-induced chemical long-term potentiation (LTP), known to evoke synaptic plasticity, or long-term depolarization block by KCl, leading to homeostatic morphological changes, we show that actin stabilization needed for the enlargement of dendritic spines is dependent on PKD activity. 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.

DOI: 10.1083/jcb.201501114

Cite this paper

@article{Bencsik2015ProteinKD, title={Protein kinase D promotes plasticity-induced F-actin stabilization in dendritic spines and regulates memory formation.}, author={Norbert Bencsik and Zs{\'o}fia Sz{\'i}ber and Hanna Liliom and Kriszti{\'a}n T{\'a}rnok and S{\'a}ndor Borb{\'e}ly and M{\'a}rton Guly{\'a}s and Anik{\'o} Erika R{\'a}tkai and Attila Szűcs and Di{\'a}na Hazai-Nov{\'a}k and Kornelia Ellwanger and Bence R{\'a}cz and Klaus Pfizenmaier and Angelika Hausser and Katalin Schlett}, journal={The Journal of cell biology}, year={2015}, volume={210 5}, pages={771-83} }