Evidence map›Paper›PMID 19579000›Full record

ArticleEuropean archives of psychiatry and clinical neuroscience2010

Risperidone and haloperidol promote survival of stem cells in the rat hippocampus.

Gerburg Keilhoff, Gisela Grecksch, Hans-Gert Bernstein, Thomas Roskoden, Axel Becker

Abstract read
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In one paragraph

Article in European archives of psychiatry and clinical neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 7% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. NMDA Receptor Model of Antipsychotic Drug-Induced Hypofrontality.International journal of molecular sciences · 2019
    Review
  8. Article
  9. Adult neurogenesis and neurodegenerative diseases: A systems biology perspective.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2017
    Article
  10. Article
  11. Article
  12. Article
  13. Adult neurogenesis and mental illness.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2015
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  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

5 authors at 1 institution in 1 country.

Gerburg KeilhoffInstitute of Biochemistry and Cell Biology, University of Magdeburg, Leipziger Strasse 44, Magdeburg, Germany. gerburg.keilhoff@med.ovgu.de
Gisela Grecksch
Hans-Gert Bernstein
Thomas Roskoden
Axel Becker
University Hospital Magdeburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Altered neuroplasticity contributes to the pathophysiology of schizophrenia. However, the idea that antipsychotics may act, at least in part, by normalizing neurogenesis has not been consistently supported. Our study seeks to determine whether hippocampal cell proliferation is altered in adult rats pretreated with ketamine, a validated model of schizophrenia, and whether chronic administration with neuroleptic drugs (haloperidol and risperidone) affect changes of cell genesis/survival. Ketamine per se has no effect on cell proliferation. Its withdrawal, however, significantly induced cell proliferation/survival in the hippocampus. Risperidone and haloperidol supported cell genesis/survival as well. During ketamine withdrawal, however, their application did not affect cell proliferation/survival additionally. TUNEL staining indicated a cell-protective potency of both neuroleptics with respect to a ketamine-induced cell death. As RT-PCR and Western blot revealed that the treatment effects of risperidone and haloperidol seemed to be mediated through activation of VEGF and MMP2. The mRNA expression of NGF, BDNF, and NT3 was unaffected. From the respective receptors, only TrkA was enhanced when ketamine withdrawal was combined with risperidone or haloperidol. Risperidone also induced BCL-2. Ketamine withdrawal has no effect on the expression of VEGF, MMP2, or BCL-2. It activated the expression of BDNF. This effect was normalized by risperidone or haloperidol. The findings indicate a promoting effect of risperidone and haloperidol on survival of young neurons in the hippocampus by enhancing the expression of the anti-apoptotic protein BCL-2 and by activation of VEGF/MMP2, whereby an interference with ketamine and thus a priority role of the NMDA system was not evident.

Indexed as

Adult Stem CellsAnimalsAntipsychotic AgentsBromodeoxyuridineCell ProliferationCell SurvivalGene Expression RegulationHaloperidolHippocampusIn Situ Nick-End LabelingMaleModels, AnimalNerve Tissue ProteinsRatsRats, Sprague-DawleyRisperidoneAntipsychotic AgentsBromodeoxyuridineHaloperidolNerve Tissue ProteinsRisperidoneRNA, Messenger

Identifiers

PMID19579000
OpenAlexW2009679143

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.