Evidence map›Paper›PMID 23001052›Full record

ArticleAnesthesiology2012

Propofol at clinically relevant concentrations increases neuronal differentiation but is not toxic to hippocampal neural precursor cells in vitro.

Jeffrey W Sall, Greg Stratmann, Jason Leong, Elliott Woodward, Philip E Bickler

Open access · bronzeAbstract read
In one paragraph

Article in Anesthesiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

30 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
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  8. Review
  9. The Effects of Propofol on a HumanFrontiers in cellular neuroscience · 2022
    Article
  10. Effects of propofol on hippocampal neuron viability.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2020
    Article
  11. Article
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  15. Propofol Alters Long Non-Coding RNA Profiles in the Neonatal Mouse Hippocampus: Implication of Novel Mechanisms in Anesthetic-Induced Developmental Neurotoxicity.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2018
    Article
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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.

Jeffrey W SallDepartment of Anesthesia and Perioperative Care, University of California, San Francisco, San Francisco, California 94143-0542, USA. sallj@anesthesia.ucsf.edu
Greg Stratmann
Jason Leong
Elliott Woodward
Philip E Bickler
Marymount University · US

Funding

Volatile anesthetic alteration of neural precursor cell cycle and fate decisionsK08GM086511 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI SALL, JEFFREY W · 2010 to 2013
$478k
NIGMS NIH HHS K08 GM086511
6 · The paper itself

Abstract

backgroundPropofol in the early postnatal period has been shown to cause brain cell death. One proposed mechanism for cognitive dysfunction after anesthesia is alteration of neural stem cell function and neurogenesis. We examined the effect of propofol on neural precursor or stem cells (NPCs) grown in vitro.

methodsHippocampal-derived NPCs from postnatal day 2 rats were exposed to propofol or Diprivan. NPCs were then analyzed for bromodeoxyuridine incorporation to measure proliferation. Cell death was measured by lactate dehydrogenase release. Immunocytochemistry was used to evaluate the expression of neuronal and glial markers in differentiating NPCs exposed to propofol.

resultsPropofol dose dependently increases the release of lactate dehydrogenase from NPCs under both proliferating and differentiating conditions at supraclinical concentrations (more than 7.1 µM). Both Diprivan and propofol had the same effect on NPCs. Propofol-mediated release of lactate dehydrogenase is not inhibited by blocking the γ-aminobutyric acid type A receptor or extracellular calcium influx and is not mediated by caspase-3/7. Direct γ-aminobutyric acid type A receptor activation did not have the same effect. In differentiating NPCs, 6 h of propofol at 2.1 µM increased the number neurons but not glial cells 4 days later. Increased neuronal differentiation was not blocked by bicuculline.

conclusionsOnly supraclinical concentrations of propofol or Diprivan kill NPCs in culture by a non-γ-aminobutyric acid type A, noncaspase-3 mechanism. Clinically relevant doses of propofol increase neuronal fate choice by a non-γ-aminobutyric acid type A mechanism.

Indexed as

AnimalsAnimals, NewbornCell DifferentiationCells, CulturedDose-Response Relationship, DrugHippocampusNeural Stem CellsNeurogenesisNeuronsPropofolRatsRats, Sprague-DawleyPropofol

Identifiers

PMID23001052
PMCPMC3483886
OpenAlexW1968473902

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.