Evidence map›Paper›PMID 23336981›Full record

ReviewNeurobiology of disease2013

Synapse-specific contributions in the cortical pathology of schizophrenia.

Saurav Seshadri, Mariela Zeledon, Akira Sawa

Open access · greenAbstract readReview
In one paragraph

Review in Neurobiology of disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

20 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Excitatory Synaptic Drive and Feedforward Inhibition in the Hippocampal CA3 Circuit Are Regulated by SynCAM 1.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Synapse-type-specific plasticity in local circuits.Current opinion in neurobiology · 2015
    Review
  12. Review
  13. Article
  14. Identification of gene ontologies linked to prefrontal-hippocampal functional coupling in the human brain.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  15. PAKs inhibitors ameliorate schizophrenia-associated dendritic spine deterioration in vitro and in vivo during late adolescence.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  16. Review
  17. Developmental origins of brain disorders: roles for dopamine.Frontiers in cellular 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

3 authors at 1 institution in 1 country.

Saurav SeshadriDepartment of Psychiatry, Johns Hopkins University, Baltimore, MD 21287, USA.
Mariela Zeledon
Akira Sawa
Johns Hopkins University · US

Funding

Project 3P50MH094268 · NIMH · JOHNS HOPKINS UNIVERSITY · PI LEEK, JEFFREY T. · 2011 to 2020
$19.9M
Predoctoral Training Program in Human GeneticsT32GM007814 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI VALLE, DAVID · 1985 to 2021
$10.6M
Research Center for Molecular Pathogenesis of SchizophreniaP20MH084018 · NIMH · JOHNS HOPKINS UNIVERSITY · PI GALLAGHER, MICHAELA · 2008 to 2010
$3.3M
Nuclear pathway of DISC1 in major mental illnesses: biochemistry and cell biologyR01MH069853 · NIMH · JOHNS HOPKINS UNIVERSITY · PI SAWA, AKIRA · 2004 to 2012
$3.2M
Oxidative stress and schizophrenia: combination of cell biology and brain imagingR01MH092443 · NIMH · JOHNS HOPKINS UNIVERSITY · PI SAWA, AKIRA · 2011 to 2015
$1.8M
Defining of Neurodevelopmental Pathways Regulated by Neuregulin- DISC1 InteractioRC1MH088753 · NIMH · UNIV OF NORTH CAROLINA CHAPEL HILL · PI ANTON, EVA S, SAWA, AKIRA · 2009 to 2010
$933k
PICK1 knockout mice: role for D-serine in neonatal forebrainsR21MH085226 · NIMH · JOHNS HOPKINS UNIVERSITY · PI SAWA, AKIRA · 2010 to 2011
$369k
NIGMS NIH HHS T32 GM007814NIMH NIH HHS MH-069853NIMH NIH HHS MH-084018NIMH NIH HHS MH-085226NIMH NIH HHS MH-088753NIMH NIH HHS MH-092443NIMH NIH HHS P20 MH084018NIMH NIH HHS P50 MH094268NIMH NIH HHS R01 MH069853NIMH NIH HHS R01 MH092443NIMH NIH HHS R21 MH085226NIMH NIH HHS RC1 MH088753
6 · The paper itself

Abstract

Schizophrenia (SZ) is often described as a disease of neuronal connectivity. Cognitive processes such as working memory, which are particularly dependent on the proper functioning of complex cortical circuitry, are disturbed in the disease. Reciprocal connections between pyramidal neurons and interneurons, as well as dopaminergic innervations, form the basis for higher cognition in the cortex. Nonetheless, only a few review articles are available which address how each synapse operates, and is possibly disturbed in SZ, at least in part by the mechanisms involving genetic susceptibility factors for SZ. In this review, we provide an overview of cortical glutamatergic, GABAergic, and dopaminergic circuitry, review SZ-associated deficits at each of these synapses, and discuss how genetic factors for SZ may contribute to SZ-related phenotype deficits in a synapse-specific manner. Pinpointing the spatially and temporally distinct sites of action of putative SZ susceptibility factors may help us better understand the pathological mechanisms of SZ, especially those associated with synaptic functioning and neuronal connectivity.

Indexed as

AnimalsCerebral CortexHumansNerve NetNeuronsPresynaptic TerminalsSchizophreniaSynapses

Identifiers

PMID23336981
PMCPMC3954843
OpenAlexW2006443952

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.