Evidence map›Paper›PMID 26304723›Full record

ArticleThe Journal of cell biology2015

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

Norbert Bencsik, Zsófia Szíber, Hanna Liliom, Krisztián Tárnok, Sándor Borbély, Márton Gulyás, Anikó Rátkai, Attila Szűcs, Diána Hazai-Novák, Kornelia Ellwanger and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.3field-weighted citation impact, top 24% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. PKD1 Promotes Functional Synapse Formation Coordinated with N-Cadherin in Hippocampus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  6. Article
  7. Fluorescence imaging of synapse dynamics in normal circuit maturation and in developmental disorders.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2017
    Review
  8. Article
  9. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors at 3 institutions in 2 countries.

Norbert BencsikDepartment of Physiology and Neurobiology, Eötvös Loránd University, H-1117 Budapest, Hungary.
Zsófia SzíberDepartment of Physiology and Neurobiology, Eötvös Loránd University, H-1117 Budapest, Hungary.
Hanna LiliomDepartment of Physiology and Neurobiology, Eötvös Loránd University, H-1117 Budapest, Hungary.
Krisztián TárnokDepartment of Physiology and Neurobiology, Eötvös Loránd University, H-1117 Budapest, Hungary.
Sándor BorbélyDepartment of Physiology and Neurobiology, Eötvös Loránd University, H-1117 Budapest, Hungary.
Márton GulyásMTA-ELTE-NAP B Neuronal Cell Biology Research Group, H-1117 Budapest, Hungary.
Anikó RátkaiDepartment of Physiology and Neurobiology, Eötvös Loránd University, H-1117 Budapest, Hungary.
Attila SzűcsMTA-ELTE-NAP B Neuronal Cell Biology Research Group, H-1117 Budapest, Hungary.
Diána Hazai-NovákDepartment of Anatomy and Histology, Faculty of Veterinary Science, Szent István University, H-1400 Budapest, Hungary.
Kornelia EllwangerInstitute of Cell Biology and Immunology, University of Stuttgart, D-70569 Stuttgart, Germany.
Bence RáczDepartment of Anatomy and Histology, Faculty of Veterinary Science, Szent István University, H-1400 Budapest, Hungary.
Klaus PfizenmaierInstitute of Cell Biology and Immunology, University of Stuttgart, D-70569 Stuttgart, Germany.
Angelika HausserInstitute of Cell Biology and Immunology, University of Stuttgart, D-70569 Stuttgart, Germany.
Katalin SchlettDepartment of Physiology and Neurobiology, Eötvös Loránd University, H-1117 Budapest, Hungary MTA-ELTE-NAP B Neuronal Cell Biology Research Group, H-1117 Budapest, Hungary schlettk@ludens.elte.hu.
Eötvös Loránd University · HUUniversity of Stuttgart · DEMagyar Agrár- és Élettudományi Egyetem · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

ActinsAnimalsCA1 Region, HippocampalCA2 Region, HippocampalCells, CulturedCell SurvivalDendritic SpinesGlycineGreen Fluorescent ProteinsLearningLong-Term PotentiationMemoryMiceMice, TransgenicNeuromuscular Depolarizing AgentsNeuronal PlasticityActinsenhanced green fluorescent proteinGlycineGreen Fluorescent ProteinsNeuromuscular Depolarizing AgentsPotassium ChlorideProtein Kinase Cprotein kinase D

Identifiers

PMID26304723
PMCPMC4555815
OpenAlexW1924168215

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.