%0 Journal Article %1 Bencsik2015 %A Bencsik, Norbert %A Szíber, Zsófia %A Liliom, Hanna %A Tárnok, Krisztián %A Borbély, Sándor %A Gulyás, Márton %A Rátkai, Anikó %A Szucs, Attila %A Hazai-Novák, Diána %A Ellwanger, Kornelia %A Rácz, Bence %A Pfizenmaier, Klaus %A Hausser, Angelika %A Schlett, Katalin %D 2015 %J Journal of Cell Biology %K 2015 hausser izi pfizenmaier %N 5 %P 771--783 %R 10.1083/jcb.201501114 %T Protein kinase D promotes plasticity-induced F-actin stabilization in dendritic spines and regulates memory formation %U http://www.ncbi.nlm.nih.gov/pubmed/26304723 %V 210 %X Actin turnover in dendritic spines influences spine development, morphology, and plasticity, with functional conse- quences on learning and memory formation. In nonneuronal cells, protein kinase D (PKD) has an important role in sta- bilizing 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. Introduction

@article{Bencsik2015, abstract = {Actin turnover in dendritic spines influences spine development, morphology, and plasticity, with functional conse- quences on learning and memory formation. In nonneuronal cells, protein kinase D (PKD) has an important role in sta- bilizing 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. Introduction}, added-at = {2023-06-29T13:07:55.000+0200}, author = {Bencsik, Norbert and Sz{\'{i}}ber, Zs{\'{o}}fia and Liliom, Hanna and T{\'{a}}rnok, Kriszti{\'{a}}n and Borb{\'{e}}ly, S{\'{a}}ndor and Guly{\'{a}}s, M{\'{a}}rton and R{\'{a}}tkai, Anik{\'{o}} and Szucs, Attila and Hazai-Nov{\'{a}}k, Di{\'{a}}na and Ellwanger, Kornelia and R{\'{a}}cz, Bence and Pfizenmaier, Klaus and Hausser, Angelika and Schlett, Katalin}, biburl = {https://puma.ub.uni-stuttgart.de/bibtex/23b14b9e8f5c015d58e5d3da4615ed3df/fabian}, doi = {10.1083/jcb.201501114}, interhash = {45f46bdf98699c99cad04c19ef4b9366}, intrahash = {3b14b9e8f5c015d58e5d3da4615ed3df}, issn = {15408140}, journal = {Journal of Cell Biology}, keywords = {2015 hausser izi pfizenmaier}, month = aug, number = 5, pages = {771--783}, pmid = {26304723}, timestamp = {2023-06-29T13:07:55.000+0200}, title = {{Protein kinase D promotes plasticity-induced F-actin stabilization in dendritic spines and regulates memory formation}}, url = {http://www.ncbi.nlm.nih.gov/pubmed/26304723}, volume = 210, year = 2015 }