Evidence map›Paper›PMID 28733355›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2017

ERK/MAPK Signaling Is Required for Pathway-Specific Striatal Motor Functions.

Scott R Hutton, James M Otis, Erin M Kim, Yashna Lamsal, Garret D Stuber, William D Snider

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

32 citing papers in PubMed, 83 citations in OpenAlex.

  1. Review
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  9. Acta pharmaceutica Sinica. B · 2024
    Review
  10. Article
  11. OncogenicNeural regeneration research · 2023
    Article
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  13. Review
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  18. Review
  19. Selective Manipulation of G-Protein γThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  20. 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

6 authors at 2 institutions in 1 country.

Scott R HuttonNeuroscience Center.
James M OtisNeuroscience Center.
Erin M KimNeuroscience Center.ORCID 0000-0002-5052-8984
Yashna LamsalNeuroscience Center.
Garret D StuberNeuroscience Center.
William D SniderNeuroscience Center, william_snider@med.unc.edu.
Beaumont Hospital, Royal Oak · USUniversity of North Carolina at Chapel Hill · US

Funding

UNC Neuroscience Center Research Cores: MicroscopyP30NS045892 · NINDS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI ZYLKA, MARK J. · 2003 to 2022
$11.5M
Roles of Growth Factor Signaling in Neural RegenerationR01NS031768 · NINDS · WASHINGTON UNIVERSITY · PI SNIDER, WILLIAM D · 1993 to 2016
$6.7M
Midbrain Neural Circuit Elements That Underlie Cue-Reward AssociationsR01DA032750 · NIDA · UNIV OF NORTH CAROLINA CHAPEL HILL · PI STUBER, GARRET D · 2012 to 2016
$1.6M
Evaluating the function and activity dynamics of thalamic inputs for reward seeking and consumptionF32DA041184 · NIDA · UNIV OF NORTH CAROLINA CHAPEL HILL · PI OTIS, JAMES M · 2016 to 2018
$144k
NIDA NIH HHS F32 DA041184NIDA NIH HHS R01 DA032750NINDS NIH HHS P30 NS045892NINDS NIH HHS R01 NS031768
6 · The paper itself

Abstract

The ERK/MAPK intracellular signaling pathway is hypothesized to be a key regulator of striatal activity via modulation of synaptic plasticity and gene transcription. However, prior investigations into striatal ERK/MAPK functions have yielded conflicting results. Further, these studies have not delineated the cell-type-specific roles of ERK/MAPK signaling due to the reliance on globally administered pharmacological ERK/MAPK inhibitors and the use of genetic models that only partially reduce total ERK/MAPK activity. Here, we generated mouse models in which ERK/MAPK signaling was completely abolished in each of the two distinct classes of medium spiny neurons (MSNs). ERK/MAPK deletion in D1R-MSNs (direct pathway) resulted in decreased locomotor behavior, reduced weight gain, and early postnatal lethality. In contrast, loss of ERK/MAPK signaling in D2R-MSNs (indirect pathway) resulted in a profound hyperlocomotor phenotype. ERK/MAPK-deficient D2R-MSNs exhibited a significant reduction in dendritic spine density, markedly suppressed electrical excitability, and suppression of activity-associated gene expression even after pharmacological stimulation. Our results demonstrate the importance of ERK/MAPK signaling in governing the motor functions of the striatal direct and indirect pathways. Our data further show a critical role for ERK in maintaining the excitability and plasticity of D2R-MSNs.

Indexed as

AnimalsCorpus StriatumFemaleLocomotionMaleMAP Kinase Signaling SystemMiceMice, Inbred C57BLMice, TransgenicMovementRandom Allocationactivity-induced gene expressionbasal gangliadendritic spinehyperlocomotionMAP kinasemedium spiny neuron

Identifiers

PMID28733355
PMCPMC5566864
OpenAlexW2739201836

What OpenQuestion holds

Textmetadata
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.