Evidence map›Paper›PMID 16131546›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2005

Regulation of synaptic plasticity in a schizophrenia model.

Barbara Gisabella, Vadim Y Bolshakov, Francine M Benes

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 2 pooled it
–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

18 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Network-based drug repurposing for schizophrenia.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024
    Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Amygdalocortical circuitry in schizophrenia: from circuits to molecules.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2010
    Review
  11. Article
  12. The evolution of drug development in schizophrenia: past issues and future opportunities.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2008
    Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Characterization of brain neurons that express enzymes mediating neurosteroid biosynthesis.Proceedings of the National Academy of Sciences of the United States of America · 2006
    Article
  18. 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

3 authors.

Barbara GisabellaProgram in Structural and Molecular Neuroscience, McLean Hospital, Belmont, MA 02478, USA.
Vadim Y Bolshakov
Francine M Benes

Funding

LTD and depotentiation in the hippocampusR01NS045625 · NINDS · MC LEAN HOSPITAL (BELMONT, MA) · PI BOLSHAKOV, VADIM · 2003 to 2006
$1.2M
Synaptic mechanisms of fear conditioningR01NS044185 · NINDS · MC LEAN HOSPITAL (BELMONT, MA) · PI BOLSHAKOV, VADIM · 2002 to 2005
$1.1M
HIPPOCAMPAL GENE EXPRESSION IN SCHIZOPHRENIAR21MH062822 · NIMH · MC LEAN HOSPITAL (BELMONT, MA) · PI BENES, FRANCINE M. · 2000 to 2001
$395k
NIMH NIH HHS MH62822NINDS NIH HHS NS045625NINDS NIH HHS NS44185NINDS NIH HHS R01 NS044185NINDS NIH HHS R01 NS045625
6 · The paper itself

Abstract

The pathology of schizophrenia is characterized by increased hippocampal activity at baseline and during auditory hallucinations. Animal-model studies in which the flow of activity to the hippocampus is increased through decreased amygdalar GABAergic inhibition have shown alterations of hippocampal circuitry similar to schizophrenia, but the functional importance of this phenomenon remains unclear. We provide evidence of decreased hippocampal feed-forward and tonic GABA-mediated inhibition in this animal model, complementing increased hippocampal activity seen in neuroimaging and postmortem studies. We demonstrate that GABA dysfunction increases long-term potentiation through activation of the cholinergic system, offering a new mechanism for pharmacological strategies of this disorder.

Indexed as

Neuronal PlasticityAnimalsDisease Models, AnimalElectrophysiologygamma-Aminobutyric AcidHippocampusMaleRatsRats, Sprague-DawleyReceptor, Muscarinic M1Receptor, Muscarinic M3Receptors, CholinergicSchizophreniagamma-Aminobutyric AcidReceptor, Muscarinic M1Receptor, Muscarinic M3Receptors, Cholinergic

Identifiers

PMID16131546
PMCPMC1201605

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.