Evidence map›Paper›PMID 23395831›Full record

ArticleNeuroscience letters2013

The blockade of NMDA receptor ion channels by ketamine is enhanced in developing rat cortical neurons.

Jianhui Jin, Kerui Gong, Xiaoju Zou, Ruirui Wang, Qing Lin, Jun Chen

Abstract read
In one paragraph

Article in Neuroscience letters, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.2field-weighted citation impact, top 14% 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

18 citing papers in PubMed, 34 citations in OpenAlex.

  1. Altered Auditory Maturation in Fragile X Syndrome and Its Involvement in Audiogenic Seizure Susceptibility.Autism research : official journal of the International Society for Autism Research · 2026
    Article
  2. Review
  3. Review
  4. Article
  5. Ketamine: Neuroprotective or Neurotoxic?Frontiers in neuroscience · 2021
    Review
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  8. Article
  9. Review
  10. Review
  11. Article
  12. 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

6 authors at 2 institutions in 2 countries.

Jianhui JinInstitute for Biomedical Sciences of Pain, Capital Medical University, Beijing, China.
Kerui Gong
Xiaoju Zou
Ruirui Wang
Qing Lin
Jun Chen
The University of Texas at Arlington · USCapital Medical University · CN

Funding

Spinal Cord-Mediated Acute Neurogenic InflammationR01NS040723 · NINDS · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI LIN, QING · 2001 to 2010
$2.3M
NINDS NIH HHS NS040723NINDS NIH HHS R01 NS040723
6 · The paper itself

Abstract

Ketamine is a non-competitive antagonist of NMDA receptors (NMDARs) commonly used as a dissociative anesthetic in many pediatric procedures. Ketamine acts primarily by blocking NMDA ligand-gated channels. Experimental studies indicate that ketamine administration used for inducing clinically relevant anesthesia can lead to neurotoxic effects, such as apoptosis, selectively on immature brain neurons. However, the underlying mechanisms remain unclear. This study used whole-cell patch-clamp recordings in an in vitro preparation of forebrain slices to analyze pharmacologically the differences in the effects of ketamine administration on the NMDAR channel activity between immature and mature neurons. NMDAR channel activity was recorded in the form of evoked NMDAR-mediated excitatory postsynaptic currents (eEPSCs) from the forebrain of both neonatal and adult rats. Results show that ketamine inhibited eEPSCs in a dose-dependent manner in both immature and mature neurons. However, at each concentration of ketamine applied to the brain slice, a more extensive inhibition could be seen in neonatal neurons than in adult neurons. Further, the blocking effect of ketamine on eEPSCs was measured during the period of 1, 3, and 6h after ketamine washout. Inhibition of eEPSCs in immature neurons was still evident 6h after washout. In contrast, the blockade of eEPSCs in mature neurons recovered completely from the inhibition by ketamine in a time-dependent manner. These results indicate that ketamine produces a greater and longer blocking effect on NMDAR channels in immature neurons than in mature neurons. This differential effect is likely to be a critical link to the higher vulnerability to ketamine-induced neurotoxicity in neurons of the developing brain.

Indexed as

Anesthetics, DissociativeAnimalsExcitatory Postsynaptic PotentialsFemaleIn Vitro TechniquesKetamineMaleNeuronsPatch-Clamp TechniquesProsencephalonRatsRats, Sprague-DawleyReceptors, N-Methyl-D-AspartateAnesthetics, DissociativeKetamineReceptors, N-Methyl-D-Aspartate

Identifiers

PMID23395831
PMCPMC3602117
OpenAlexW2062620314

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.