Evidence map›Paper›PMID 23113835›Full record

ArticleJournal of neurochemistry2013

Protease-activated receptor-1 modulates hippocampal memory formation and synaptic plasticity.

Antoine G Almonte, Laura H Qadri, Faraz A Sultan, Jennifer A Watson, Daniel J Mount, Gavin Rumbaugh, J David Sweatt

Abstract read
In one paragraph

Article in Journal of neurochemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
–field-weighted citation impact
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

31 citing papers in PubMed.

  1. Mechanistic insights into the liver-brain axis during chronic liver disease.Nature reviews. Gastroenterology & hepatology · 2026
    Review
  2. CD103Nature communications · 2025
    Article
  3. Article
  4. Diversification of PAR signaling through receptor crosstalk.Cellular & molecular biology letters · 2022
    Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. A Role for Matrix Metalloproteases in Antidepressant Efficacy.Frontiers in molecular neuroscience · 2019
    Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Review
  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

7 authors.

Antoine G AlmonteDepartment of Neurobiology and Evelyn F. McKnight Brain Institute, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Laura H Qadri
Faraz A Sultan
Jennifer A Watson
Daniel J Mount
Gavin Rumbaugh
J David Sweatt

Funding

Intersection of causal neurodevelopmental disorder risk genes, cortical circuit function, and cognitive processing required for behavioral adaptionsR01MH096847 · NIMH · UNIVERSITY OF FLORIDA · PI Courtney A Miller, GAVIN R RUMBAUGH · 2012 to 2026
$10.4M
Alabama Neuroscience Blueprint Core CenterP30NS057098 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI SWEATT, JOHN DAVID · 2006 to 2010
$9.5M
Biochemical Mechanisms of Neural PlasticityR01MH057014 · NIMH · VANDERBILT UNIVERSITY · PI WINDER, DANNY G. · 1996 to 2019
$9.3M
Regulation of Memory Formation by the GTPase-activating Protein SynGAPR01NS064079 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI RUMBAUGH, GAVIN R · 2009 to 2017
$3.9M
DNA Methylation in Memory FormationR01MH091122 · NIMH · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI SWEATT, JOHN DAVID · 2011 to 2015
$1.8M
Trophic Interactions of Nerve and MuscleR01AG031722 · NIA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI SWEATT, JOHN DAVID · 2007 to 2011
$1.6M
NIA NIH HHS AG031722NIA NIH HHS R01 AG031722NIMH NIH HHS MH57014NIMH NIH HHS R01 MH057014NIMH NIH HHS R01 MH091122NIMH NIH HHS R01 MH096847NINDS NIH HHS NS057098NINDS NIH HHS P30 NS057098NINDS NIH HHS R01 NS064079
6 · The paper itself

Abstract

Protease-activated receptor-1 (PAR1) is an unusual G-protein coupled receptor (GPCR) that is activated through proteolytic cleavage by extracellular serine proteases. Although previous work has shown that inhibiting PAR1 activation is neuroprotective in models of ischemia, traumatic injury, and neurotoxicity, surprisingly little is known about PAR1's contribution to normal brain function. Here, we used PAR1-/- mice to investigate the contribution of PAR1 function to memory formation and synaptic function. We demonstrate that PAR1-/- mice have deficits in hippocampus-dependent memory. We also show that while PAR1-/- mice have normal baseline synaptic transmission at Schaffer collateral-CA1 synapses, they exhibit severe deficits in N-methyl-d-aspartate receptor (NMDAR)-dependent long-term potentiation (LTP). Mounting evidence indicates that activation of PAR1 leads to potentiation of NMDAR-mediated responses in CA1 pyramidal cells. Taken together, this evidence and our data suggest an important role for PAR1 function in NMDAR-dependent processes subserving memory formation and synaptic plasticity.

Indexed as

6-Cyano-7-nitroquinoxaline-2,3-dioneAction PotentialsAnimalsBiophysicsConditioning, PsychologicalElectric StimulationExcitatory Amino Acid AntagonistsExcitatory Postsynaptic PotentialsFearHippocampusIn Vitro TechniquesLong-Term PotentiationMemoryMemory DisordersMiceMice, Inbred C57BL6-Cyano-7-nitroquinoxaline-2,3-dioneExcitatory Amino Acid AntagonistsReceptor, PAR-1RNA, Messenger

Identifiers

PMID23113835
PMCPMC3518655

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.