Evidence map›Paper›PMID 19396876›Full record

ArticleJournal of neuroscience research2009

N-methyl-D-aspartate-stimulated ERK1/2 signaling and the transcriptional up-regulation of plasticity-related genes are developmentally regulated following in vitro neuronal maturation.

Xianju Zhou, Changjong Moon, Fei Zheng, Yongneng Luo, Deborah Soellner, Joseph L Nuñez, Hongbing Wang

Open access · greenAbstract read
In one paragraph

Article in Journal of neuroscience research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
1.5field-weighted citation impact, top 21% 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

37 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
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  7. Ribosome heterogeneity in development and disease.Frontiers in cell and developmental biology · 2024
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  13. Astrocytic cAMP modulates memory via synaptic plasticity.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
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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

7 authors at 1 institution in 2 countries.

Xianju ZhouDepartment of Physiology, Michigan State University, East Lansing, Michigan 48824, USA.
Changjong Moon
Fei Zheng
Yongneng Luo
Deborah Soellner
Joseph L Nuñez
Hongbing Wang
Michigan State University · US

Funding

Regulation of BDNF Expression by Calcium-stimulated Protein KinasesR01MH076906 · NIMH · MICHIGAN STATE UNIVERSITY · PI WANG, HONGBING · 2007 to 2010
$1.2M
Novel GABA Actions on the Developing BrainK01MH068347 · NIMH · UNIVERSITY OF MARYLAND BALTIMORE · PI NUNEZ, JOSEPH LUIS · 2004 to 2008
$695k
NIDA NIH HHS F31DA02378NIMH NIH HHS K01 MH068347NIMH NIH HHS MH068347NIMH NIH HHS MH076906NIMH NIH HHS R01 MH076906
6 · The paper itself

Abstract

The general features of neuroplasticity are developmentally regulated. Although it has been hypothesized that the loss of plasticity in mature neurons may be due to synaptic saturation and functional reduction of N-methyl-D-aspartate receptors (NMDAR), the molecular mechanisms remain largely unknown. We examined the effects of NMDAR activation and KCl-mediated membrane depolarization on ERK1/2 signaling following in vitro maturation of cultured cortical neurons. Although NMDA stimulated a robust increase in intracellular calcium at both DIV (day in vitro) 3 and 14, the activation of ERK1/2 and cAMP responsive element-binding protein (CREB) was impaired at DIV 14. Specifically, the phosphorylation of ERK1/2 was stimulated by both NMDA and KCl at DIV 3. However, at DIV 14, NMDA- but not KCl-stimulated ERK1/2 and CREB phosphorylation was significantly diminished. Consistently, the NMDA-induced transcription of ERK/CREB-regulated genes Bdnf exon 4, Arc, and zif268 was significantly attenuated at DIV 14. Moreover, in comparison with 3 DIV neurons, the phosphorylated-ERK1/2 in 14 DIV neurons displayed a tremendous increase following maturation and was more susceptible to dephosphorylation. Blocking calcium channels by nifedipine or NMDAR by APV caused a more dramatic ERK dephosphorylation in 14 DIV neurons. We further demonstrate that the loss of plasticity-related signaling is unrelated to NMDA-induced cell death of the 14 DIV neurons. Taken together, these results suggest that the attenuation of certain aspects of neuroplasticity following maturation may be due to the reduction of NMDAR-mediated gene transcription and a saturation of ERK1/2 activity.

Indexed as

AnimalsAnimals, NewbornCalcium Channel BlockersCell DifferentiationCells, CulturedCerebral CortexCyclic AMP Response Element-Binding ProteinGene Expression Regulation, DevelopmentalMitogen-Activated Protein Kinase 3NeurogenesisNeuronal PlasticityNeuronsPhosphorylationRatsRats, Sprague-DawleyReceptors, N-Methyl-D-AspartateCalcium Channel BlockersCyclic AMP Response Element-Binding ProteinMitogen-Activated Protein Kinase 3Receptors, N-Methyl-D-Aspartate

Identifiers

PMID19396876
PMCPMC2857719
OpenAlexW2106568723

What OpenQuestion holds

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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.