Evidence map›Paper›PMID 20392954›Full record

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

RIM1alpha and interacting proteins involved in presynaptic plasticity mediate prepulse inhibition and additional behaviors linked to schizophrenia.

Jacqueline Blundell, Pascal S Kaeser, Thomas C Südhof, Craig M Powell

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 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing 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

33 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Beyond vertebrates:Frontiers in psychiatry · 2025
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Active Zone Proteins RIM1αβ Are Required for Normal Corticostriatal Transmission and Action Control.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  13. Article
  14. Review
  15. Article
  16. Genetic background effects in Neuroligin-3 mutant mice: Minimal behavioral abnormalities on C57 background.Autism research : official journal of the International Society for Autism Research · 2018
    Article
  17. Article
  18. Review
  19. Novel Shank3 mutant exhibits behaviors with face validity for autism and altered striatal and hippocampal function.Autism research : official journal of the International Society for Autism Research · 2017
    Article
  20. Altered Striatal Synaptic Function and Abnormal Behaviour in Shank3 Exon4-9 Deletion Mouse Model of Autism.Autism research : official journal of the International Society for Autism Research · 2016
    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

4 authors at 2 institutions in 1 country.

Jacqueline BlundellDepartments of Neurology and Psychiatry, The University of Texas Southwestern Medical Center, Dallas, Texas, 75390-8813, USA.
Pascal S Kaeser
Thomas C Südhof
Craig M Powell
Stanford University · USThe University of Texas Southwestern Medical Center · US

Funding

Neuroligin Function in vivo: Implications for Autism and Mental RetardationR01MH081164 · NIMH · UT SOUTHWESTERN MEDICAL CENTER · PI POWELL, CRAIG M · 2009 to 2013
$1.9M
BDNF in depression, antidepressant action, and memory.K08MH065975 · NIMH · UT SOUTHWESTERN MEDICAL CENTER · PI POWELL, CRAIG M · 2003 to 2007
$858k
Novel Genetic Animal Models of AutismR21HD065290 · NICHD · UT SOUTHWESTERN MEDICAL CENTER · PI POWELL, CRAIG M · 2009 to 2010
$550k
Howard Hughes Medical InstituteNICHD NIH HHS R21 HD065290NIMH NIH HHS K08 MH065975NIMH NIH HHS R01 MH081164
6 · The paper itself

Abstract

Several presynaptic proteins involved in neurotransmitter release in the CNS have been implicated in schizophrenia in human clinical genetic studies, in postmortem studies, and in studies of putative animal models of schizophrenia. The presynaptic protein RIM1alpha mediates presynaptic plasticity and cognitive function. We now demonstrate that mice deficient in RIM1alpha exhibit abnormalities in multiple schizophrenia-relevant behavioral tasks including prepulse inhibition, response to psychotomimetic drugs, and social interaction. These schizophrenia-relevant behavioral findings are relatively selective to RIM1alpha-deficient mice, as mice bearing mutations in the RIM1alpha binding partners Rab3A or synaptotagmin 1 only show decreased prepulse inhibition. In addition to RIM1alpha's involvement in multiple behavioral abnormalities, these data suggest that alterations in presynaptic forms of short-term plasticity are linked to alterations in prepulse inhibition, a measure of sensorimotor gating.

Indexed as

Social BehaviorAnimalsCognitionDizocilpine MaleateFemaleGTP-Binding ProteinsHallucinogensImpulsive BehaviorMaleMiceMice, Inbred C57BLMice, TransgenicMotor ActivityMutationNeuronal PlasticityPresynaptic TerminalsDizocilpine MaleateGTP-Binding ProteinsHallucinogensrab3A GTP-Binding ProteinRims1 protein, mouseSynaptotagmin ISyt1 protein, mouse

Identifiers

PMID20392954
PMCPMC2860606
OpenAlexW2013581906

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.