Evidence map›Paper›PMID 19936716›Full record

ArticlePsychopharmacology2010

Chronic administration of atypical antipsychotics improves behavioral and synaptic defects of STOP null mice.

David Delotterie, Geoffrey Ruiz, Jacques Brocard, Annie Schweitzer, Corinne Roucard, Yann Roche, Marie-Françoise Suaud-Chagny, Karine Bressand, Annie Andrieux

Open access · greenAbstract read
In one paragraph

Article in Psychopharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 2 pooled it
1.6field-weighted citation impact, top 20% 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

22 citing papers in PubMed, 2 syntheses or guidelines pooled it, 50 citations in OpenAlex.

  1. Pooled it
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  17. Postmortem brain: an underutilized substrate for studying severe mental illness.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2014
    Review
  18. Article
  19. Article
  20. Deletion of CB2 cannabinoid receptor induces schizophrenia-related behaviors in mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2011
    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

9 authors at 4 institutions in 1 country.

David DelotterieSynapCell SAS, Bâtiment Biopolis, 5 avenue du Grand Sablon, 38700, La Tronche, France.
Geoffrey Ruiz
Jacques Brocard
Annie Schweitzer
Corinne Roucard
Yann Roche
Marie-Françoise Suaud-Chagny
Karine Bressand
Annie Andrieux
Institut de Recherches en Technologies et Sciences pour le Vivant · FRInserm · FRUniversité Claude Bernard Lyon 1 · FRUniversité Joseph Fourier · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionRecent studies have suggested that schizophrenia is associated with alterations in the synaptic connectivity involving cytoskeletal proteins. The microtubule-associated protein stable tubule only polypeptide (STOP) plays a key role in neuronal architecture and synaptic plasticity, and it has been demonstrated that STOP gene deletion in mice leads to a phenotype mimicking aspects of positive and negative symptoms and cognitive deficits classically observed in schizophrenic patients. In STOP null mice, behavioral defects are associated with synaptic plasticity abnormalities including defects in long-term potentiation. In these mice, long-term administration of typical antipsychotics has been shown to partially alleviate behavioral defects but, as in humans, such a treatment was poorly active on deficits related to negative symptoms and cognitive impairments. Here, we assessed the effects of risperidone and clozapine, two atypical antipsychotics, on STOP null mice behavior and synaptic plasticity.

resultsLong-term administration of either drug results in alleviation of behavioral alterations mimicking some negative symptoms and partial amelioration of some cognitive defects in STOP null mice. Interestingly, clozapine treatment also improves synaptic plasticity of the STOP null animals by restoring long-term potentiation in the hippocampus. DISCUSSION: All together, the pharmacological reactivity of STOP null mice to antipsychotics evokes the pharmacological response of humans to such drugs. Totally, our study suggests that STOP null mice may provide a useful preclinical model to evaluate pharmacological properties of antipsychotic drugs.

Indexed as

AnimalsAntipsychotic AgentsBehavior, AnimalClozapineDrug Evaluation, PreclinicalHippocampusMaleMiceMice, KnockoutMicrotubule-Associated ProteinsNeuronal PlasticityRisperidoneAntipsychotic AgentsClozapineMicrotubule-Associated ProteinsMtap6 protein, mouseRisperidone

Identifiers

PMID19936716
PMCPMC2874572
OpenAlexW2050841927

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.