Evidence map›Paper›PMID 21195751›Full record

ArticleNeuroscience2011

Genetic disruption of Met signaling impairs GABAergic striatal development and cognition.

G J Martins, M Shahrokh, E M Powell

Abstract read
In one paragraph

Article in Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

26 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
  2. Article
  3. The role of neuroactive steroids in tic disorders.Neuroscience and biobehavioral reviews · 2024
    Review
  4. Cyclic Peptide-Based Biologics Regulating HGF-MET.International journal of molecular sciences · 2020
    Review
  5. Article
  6. Semaphorin4D Induces Inhibitory Synapse Formation by Rapid Stabilization of Presynaptic Boutons via MET Coactivation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  7. Article
  8. Estrogen Treatment Reverses Prematurity-Induced Disruption in Cortical Interneuron Population.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  9. Cortical interneuron development: a tale of time and space.Development (Cambridge, England) · 2017
    Review
  10. Review
  11. Article
  12. Insulin-Independent GABAA Receptor-Mediated Response in the Barrel Cortex of Mice with Impaired Met Activity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. 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

3 authors at 1 institution in 1 country.

G J MartinsProgram in Neuroscience, University of Maryland, Baltimore, MD 21201, USA.
M Shahrokh
E M Powell
University of Maryland, Baltimore · US

Funding

Mechanisms of Forebrain DevelopmentR01DA018826 · NIDA · UNIVERSITY OF MARYLAND BALTIMORE · PI POWELL, ELIZABETH M · 2006 to 2010
$1.4M
Autism Speaks AS1640NIDA NIH HHS R01 DA018826NIDA NIH HHS R01DA018826
6 · The paper itself

Abstract

The largest structure of the basal ganglia, the striatum, modulates motor activity and cognitive function and is composed of GABAergic projection neurons and interneurons. To better understand the mechanisms underlying the development of the striatal neurons and their assembly into functional circuits, we used a mouse with a targeted conditional Met mutation in post-mitotic cells of the ventral telencephalon. Characterization of the ontogeny of the striatal neuronal populations demonstrated that disruption of Met signaling specifically altered the GABAergic interneurons. Medium spiny neurons (MSNs) and cholinergic interneurons were largely unaffected. Mice lacking Met signaling have increased numbers of striatal GABAergic interneurons in the lateral sensorimotor areas with distinct behavioral deficits. Motor function and memory formation and consolidation appeared intact, but procedural learning on the cued task of the Morris water maze was delayed. MET is a susceptibility gene in Tourette syndrome and autism, which are human disorders with impaired procedural learning. This study reveals how a striatal targeted disruption in Met signaling after generation of striatal neurons produces behavioral phenotypes shared by Tourette syndrome and autism, linking the human genetics with the mechanism underlying the disorders.

Indexed as

AnimalsBlotting, WesternCognitionCorpus Striatumgamma-Aminobutyric AcidImmunohistochemistryInterneuronsMaze LearningMiceMice, Inbred C57BLMice, Mutant StrainsProto-Oncogene Proteins c-metSignal Transductiongamma-Aminobutyric AcidProto-Oncogene Proteins c-met

Identifiers

PMID21195751
PMCPMC3040282
OpenAlexW2038405774

What OpenQuestion holds

Textmetadata
LicenceTDM
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.