Evidence map›Paper›PMID 22635046›Full record

ArticleCritical care medicine2012

Ketamine alters the neurogenesis of rat cortical neural stem progenitor cells.

Chaoxuan Dong, Cynthia R Rovnaghi, K J S Anand

Open access · greenAbstract read
In one paragraph

Article in Critical care medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

35 citing papers in PubMed, 78 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Rapid-acting antidepressants and the circadian clock.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2022
    Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 3 institutions in 1 country.

Chaoxuan DongDepartment of Pediatrics, University of Tennessee Health Science Center, Memphis, TN, USA.
Cynthia R Rovnaghi
K J S Anand
Arkansas Children's Hospital · USUniversity of Arkansas for Medical Sciences · USUniversity of Tennessee Health Science Center · US

Funding

PCCM Network: Remedies for Opioid Tolerance &WithdrawalU10HD050009 · NICHD · ARKANSAS CHILDREN'S HOSPITAL RES INST · PI SANDERS, RONALD C · 2005 to 2009
$1.7M
NICHD NIH HHS U10 HD050009NICHD NIH HHS U10-HD50009
6 · The paper itself

Abstract

objectiveHigh doses or prolonged exposure to ketamine increase neuronal apoptosis in the developing brain, although effects on neural stem progenitor cells remain unexplored. This study investigated dose- and time-dependent responses to ketamine on cell death and neurogenesis in cultured rat fetal cortical neural stem progenitor cells.

designLaboratory-based study.

settingUniversity research laboratory. SUBJECT: Sprague-Dawley rats.

interventionsNeural stem progenitor cells were isolated from the cortex of Sprague-Dawley rat fetuses on embryonic day 17. In dose-response experiments, cultured neural stem progenitor cells were exposed to different concentrations of ketamine (0-100 µM) for 24 hrs. In time-course experiments, neural stem progenitor cells cultures were exposed to 10 µM ketamine for different durations (0-48 hrs). MEASUREMENTS AND MAIN

resultsApoptosis and necrosis in neural stem progenitor cells were assessed using activated caspase-3 immunostaining and lactate dehydrogenase assays, respectively. Proliferative changes in neural stem progenitor cells were detected using bromo-deoxyuridine incorporation and Ki67 immunostaining. Neuronal differentiation was assessed using Tuj-1 immunostaining. Cultured neural stem progenitor cells were resistant to apoptosis and necrosis following all concentrations and durations of ketamine exposure tested. Ketamine inhibited proliferation with decreased numbers of bromo-deoxyuridine-positive cells following ketamine exposure to 100 µM for 24 hrs (p<.005) or 10 µM for 48 hrs (p< .01), and reduced numbers of Ki67-positive cells following exposure to ketamine concentration>10 µM for 24 hrs (p<.001) or at 10 µM for 48 hrs (p<.01). Ketamine enhanced neuronal differentiation, with all ketamine concentrations increasing Tuj-1-positive neurons (p<.001) after 24-hrs of exposure. This also occurred with all exposures to 10 µM ketamine for >8 hrs (p<.001).

conclusionsClinically relevant concentrations of ketamine do not induce cell death in neural stem progenitor cells via apoptosis or necrosis. Ketamine alters the proliferation and increases the neuronal differentiation of neural stem progenitor cells isolated from the rat neocortex. These studies imply that ketamine exposure during fetal or neonatal life may alter neurogenesis and subsequent brain development.

Indexed as

AnimalsApoptosisCell DeathCell ProliferationCerebral CortexDose-Response Relationship, DrugKetamineNeural Stem CellsNeurogenesisRatsRats, Sprague-DawleyReceptors, N-Methyl-D-AspartateTime FactorsKetamineReceptors, N-Methyl-D-Aspartate

Identifiers

PMID22635046
PMCPMC3507468
OpenAlexW2051700776

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.