Evidence map›Paper›PMID 20427661›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010

Canonical TGF-beta signaling is required for the balance of excitatory/inhibitory transmission within the hippocampus and prepulse inhibition of acoustic startle.

Mu Sun, Jonathan C Gewirtz, Lisa Bofenkamp, Robert J Wickham, Hong Ge, Michael B O'Connor

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. 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
1.9field-weighted citation impact, top 15% 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, 51 citations in OpenAlex.

  1. Article
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  4. Article
  5. Fine-Tuning the TGFβ Signaling Pathway by SARA During Neuronal Development.Frontiers in cell and developmental biology · 2020
    Article
  6. Article
  7. Review
  8. Canonical TGF-β Signaling Negatively Regulates Neuronal Morphogenesis through TGIF/Smad Complex-Mediated CRMP2 Suppression.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  9. Article
  10. Astrocyte Transforming Growth Factor Beta 1 Protects Synapses against Aβ Oligomers in Alzheimer's Disease Model.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  11. Review
  12. Article
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  14. Article
  15. Article
  16. Article
  17. Growth factors in synaptic function.Frontiers in synaptic neuroscience · 2013
    Review
  18. Article
  19. 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 4 institutions in 2 countries.

Mu SunDepartment of Genetics, Cell Biology and Development, Howard Hughes Medical Institute, University of Minnesota, Minnesota 55455, USA.
Jonathan C Gewirtz
Lisa Bofenkamp
Robert J Wickham
Hong Ge
Michael B O'Connor
University of Minnesota · USHoward Hughes Medical Institute · USInstitut thématique Génétique, génomique et bioinformatique · FRTwin Cities Orthopedics · US

Funding

Howard Hughes Medical Institute
6 · The paper itself

Abstract

Smad4 is a unique nuclear transducer for all TGF-beta signaling pathways and regulates gene transcription during development and tissue homeostasis. To elucidate the postnatal role of TGF-beta signaling in the mammalian brain, we generated forebrain-specific Smad4 knock-out mice. Surprisingly, the mutants showed no alteration in long-term potentiation and water maze, suggesting that Smad4 is not required for spatial learning and memory. However, these mutant mice did show enhancement of paired-pulse facilitation in excitatory synaptic transmission and stronger paired-pulse depression of GABA(A) currents in the hippocampus. The alteration of hippocampal electrophysiology correlated with mouse hyperactivity in homecage and open field tests. Mutant mice also showed overgrooming as well as deficits of prepulse inhibition, a widely used endophenotype of schizophrenia. With a specific real-time PCR array focused on TGF-beta signaling pathway, we identified a novel regulation mechanism of the pathway in the hippocampal neurons, in which Smad4-mediated signaling suppresses the level of extracellular antagonism of TGF-beta ligands through transcriptional regulation of follistatin, a selective inhibitor to activin/TGF-beta signaling in the hippocampus. In summary, we suggest that the canonical TGF-beta signaling pathway is critical for use-dependent modulation of GABA(A) synaptic transmission and dendritic homeostasis; furthermore, a disruption in the balance of the excitatory and inhibitory hippocampal network can result in psychiatric-like behavior.

Indexed as

AnimalsAuditory PerceptionFollistatinHippocampusInhibin-beta SubunitsLong-Term PotentiationMaleMaze LearningMemoryMiceMice, KnockoutMotor ActivityNeural InhibitionProsencephalonReceptors, GABA-AReflex, StartleFollistatininhibin beta A subunitInhibin-beta SubunitsReceptors, GABA-ASmad4 ProteinSmad4 protein, mouseTransforming Growth Factor beta

Identifiers

PMID20427661
PMCPMC6632596
OpenAlexW1977219816

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.