Evidence map›Paper›PMID 24446171›Full record

ArticleHippocampus2014

Dysbindin-1 loss compromises NMDAR-dependent synaptic plasticity and contextual fear conditioning.

W Bailey Glen, Bryant Horowitz, Gregory C Carlson, Tyrone D Cannon, Konrad Talbot, J David Jentsch, Antonieta Lavin

Open access · greenAbstract read
In one paragraph

Article in Hippocampus, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

25 citing papers in PubMed, 30 citations in OpenAlex.

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  17. Dysbindin-1 Involvement in the Etiology of Schizophrenia.International journal of molecular sciences · 2017
    Review
  18. Article
  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

7 authors at 5 institutions in 2 countries.

W Bailey GlenDepartment of Neurosciences, Medical University of South Carolina, Charleston, South Carolina.
Bryant Horowitz
Gregory C Carlson
Tyrone D Cannon
Konrad Talbot
J David Jentsch
Antonieta Lavin
Medical University of South Carolina · USUniversity of Pennsylvania · USInstitut des Sciences Cognitives Marc Jeannerod · FRUniversity of California, Los Angeles · USYale University · US

Funding

Theta and Gamma Oscillations in Cortical MicrocircuitsP50MH064045 · NIMH · UNIVERSITY OF PENNSYLVANIA · PI GUR, RAQUEL E · 2001 to 2010
$21.6M
Translational Methods/Facilities Core (TMF - Core) (8 of 8)PL1NS062410 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI EVANS, CHRISTOPHER J. · 2007 to 2011
$4.6M
Consortium for Neuropsychiatric Phenomics-Coordinating Center (1 of 8)UL1DE019580 · NIDCR · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BILDER, ROBERT M · 2008 to 2011
$1.9M
Memory Mechanisms and Mental DisordersRL1MH083269 · NIMH · YALE UNIVERSITY · PI CANNON, TYRONE D · 2007 to 2011
$1.8M
Neurobiology of Dysbindin in Schizophrenia and sdy MouseR01MH072880 · NIMH · UNIVERSITY OF PENNSYLVANIA · PI ARNOLD, STEVEN E · 2005 to 2008
$1.7M
NIDCR NIH HHS UL1 DE-019580NIDCR NIH HHS UL1 DE019580NIMH NIH HHS P50 MH-064045NIMH NIH HHS P50 MH064045NIMH NIH HHS R01 MH-072880NIMH NIH HHS R01 MH072880NIMH NIH HHS RL1 MH083269NIMH NIH HHS RL1 MH-83269NINDS NIH HHS PL1 NS-062410NINDS NIH HHS PL1 NS062410
6 · The paper itself

Abstract

Genetic variants in DTNBP1 encoding the protein dysbindin-1 have often been associated with schizophrenia and with the cognitive deficits prominent in that disorder. Because impaired function of the hippocampus is thought to play a role in these memory deficits and because NMDAR-dependent synaptic plasticity in this region is a proposed biological substrate for some hippocampal-dependent memory functions in schizophrenia, we hypothesized that reduced dysbindin-1 expression would lead to impairments in NMDAR-dependent synaptic plasticity and in contextual fear conditioning. Acute slices from male mice carrying 0, 1, or 2 null mutant alleles of the Dtnbp1 gene were prepared, and field recordings from the CA1 striatum radiatum were obtained before and after tetanization of Schaffer collaterals of CA3 pyramidal cells. Mice homozygous for the null mutation in Dtnbp1 exhibited significantly reduced NMDAR-dependent synaptic potentiation compared to wild type mice, an effect that could be rescued by bath application of the NMDA receptor coagonist glycine (10 μM). Behavioral testing in adult mice revealed deficits in hippocampal memory processes. Homozygous null mice exhibited lower conditional freezing, without a change in the response to shock itself, indicative of a learning and memory deficit. Taken together, these results indicate that a loss of dysbindin-1 impairs hippocampal plasticity which may, in part, explain the role dysbindin-1 plays in the cognitive impairments of schizophrenia.

Indexed as

Analysis of VarianceAnimalsBiophysicsCarrier ProteinsConditioning, PsychologicalDysbindinDystrophin-Associated ProteinsElectric StimulationExcitatory Amino Acid AgentsFearFreezing Reaction, CatalepticHippocampusIn Vitro TechniquesLong-Term PotentiationMaleMiceCarrier ProteinsDtnbp1 protein, mouseDysbindinDystrophin-Associated ProteinsExcitatory Amino Acid AgentsReceptors, N-Methyl-D-Aspartatebehaviorelectrophysiologygenetic modelrodentschizophrenia

Identifiers

PMID24446171
PMCPMC3937842
OpenAlexW1955397606

What OpenQuestion holds

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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.