Evidence map›Paper›PMID 23201445›Full record

ArticleBrain research2013

Amphetamine increases phosphorylation of MAPK/ERK at synaptic sites in the rat striatum and medial prefrontal cortex.

Li-Min Mao, James M Reusch, Eugene E Fibuch, Zhenguo Liu, John Q Wang

Abstract readComparative Study
In one paragraph

Article in Brain research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.0field-weighted citation impact, top 28% 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

23 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Article
  3. Roles of adenosine ABrain and behavior · 2021
    Article
  4. The Role of CaMKII and ERK Signaling in Addiction.International journal of molecular sciences · 2021
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Local substrates of non-receptor tyrosine kinases at synaptic sites in neurons.Sheng li xue bao : [Acta physiologica Sinica] · 2017
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Molecular Mechanism: ERK Signaling, Drug Addiction, and Behavioral Effects.Progress in molecular biology and translational science · 2016
    Review
  19. Article
  20. Review
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

5 authors at 2 institutions in 2 countries.

Li-Min MaoDepartment of Basic Medical Science, School of Medicine, University of Missouri-Kansas City, Kansas City, MO 64108, USA.
James M Reusch
Eugene E Fibuch
Zhenguo Liu
John Q Wang
University of Missouri–Kansas City · USShanghai Jiao Tong University · CN

Funding

REGULATION OF GENE EXPRESSION IN STRIATAL NEURONSR01MH061469 · NIMH · UNIVERSITY OF MISSOURI KANSAS CITY · PI WANG, QIANG · 2001 to 2024
$7.9M
Metabotropic Glutamate Regulation of Amphetamine ActionR01DA010355 · NIDA · UNIVERSITY OF MISSOURI KANSAS CITY · PI WANG, QIANG · 2003 to 2017
$4.6M
NIDA NIH HHS R01 DA010355NIDA NIH HHS R01DA10355NIMH NIH HHS R01 MH061469NIMH NIH HHS R01MH61469
6 · The paper itself

Abstract

Mitogen-activated protein kinases (MAPKs) play a central role in cell signaling. Extracellular signal-regulated kinase (ERK) is a prototypic subclass of MAPKs and is densely expressed in postmitotic neurons of adult mammalian brains. Active ERK translocates into the nucleus to regulate gene expression. Additionally, ERK is visualized in neuronal peripheries, such as distal synaptic structures. While nuclear ERK is a known sensitive target of psychostimulants, little is known about the responsiveness of synaptic ERK to stimulants. In this study, we focused on ERK at synaptic versus extrasynaptic sites and investigated its responses to the psychostimulant amphetamine in the adult rat striatum and medial prefrontal cortex (mPFC) in vivo. We used a pre-validated biochemical fractionation procedure to isolate synapse- and extrasynapse-enriched membranes. We found that two common ERK isoforms (ERK1 and ERK2) were concentrated more in extrasynaptic fractions than in synaptic fractions in striatal and cortical neurons under normal conditions. At synaptic sites, ERK2 was noticeably more abundant than ERK1. Acute injection of amphetamine induced an increase in ERK2 phosphorylation in the synaptic fraction of striatal neurons, while the drug did not alter extrasynaptic ERK2 phosphorylation. Similar results were observed in the mPFC. In both synaptic and extrasynaptic compartments, total ERK1/2 proteins remained stable in response to amphetamine. Our data establish the subsynaptic distribution pattern of MAPK/ERK in striatal and cortical neurons. Moreover, the synaptic pool of ERK2 in these neurons can be selectively activated by amphetamine.

Indexed as

AnimalsCentral Nervous System StimulantsCorpus StriatumDextroamphetamineIsoenzymesMaleMAP Kinase Signaling SystemMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3PhosphorylationPrefrontal CortexRatsRats, WistarSignal TransductionSynaptic MembranesCentral Nervous System StimulantsDextroamphetamineIsoenzymesMAPK1 protein, humanMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3

Identifiers

PMID23201445
PMCPMC3546198
OpenAlexW2083781846

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.