Evidence map›Paper›PMID 39746093›Full record

ArticlePloS one2025

Effects of ketamine and propofol on muscarinic plateau potentials in rat neocortical pyramidal cells.

Anne S Fleiner, Daniel Kolnier, Nicholas Hagger-Vaughan, Johan Ræder, Johan F Storm

Abstract read
In one paragraph

Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Article
  2. Review
  3. 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.

Anne S FleinerDepartment of Molecular Medicine, Brain Signalling Laboratory, Institute of Basic Medical Sciences, Section for Physiology, University of Oslo, Oslo, Norway.ORCID 0009-0008-3867-2431
Daniel KolnierDepartment of Molecular Medicine, Brain Signalling Laboratory, Institute of Basic Medical Sciences, Section for Physiology, University of Oslo, Oslo, Norway.ORCID 0009-0004-3196-7051
Nicholas Hagger-VaughanDepartment of Molecular Medicine, Brain Signalling Laboratory, Institute of Basic Medical Sciences, Section for Physiology, University of Oslo, Oslo, Norway.
Johan RæderInstitute of Clinical Medicine, University of Oslo, Oslo, Norway.
Johan F StormDepartment of Molecular Medicine, Brain Signalling Laboratory, Institute of Basic Medical Sciences, Section for Physiology, University of Oslo, Oslo, Norway.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Propofol and ketamine are widely used general anaesthetics, but have different effects on consciousness: propofol gives a deeply unconscious state, with little or no dream reports, whereas vivid dreams are often reported after ketamine anaesthesia. Ketamine is an N-methyl-D-aspartate (NMDA) receptor antagonist, while propofol is a γ-aminobutyric-acid (GABAA) receptor positive allosteric modulator, but these mechanisms do not fully explain how these drugs alter consciousness. Most previous in vitro studies of cellular mechanisms of anaesthetics have used brain slices or neurons in a nearly "comatose" state, because no "arousing" neuromodulators were added. Here we tested mechanisms of anaesthetics in rat medial prefrontal cortex (mPFC) slices after bath-applying the cholinergic agonist muscarine to partly mimic an "aroused-like" state, using whole-cell patch-clamp recordings from layer 2/3 pyramidal cells (L2/3PCs). According to leading theories of access consciousness and working memory, L2/3PCs are particularly important for these cognitive functions. We found that muscarine induced long-lasting depolarising plateau potentials (PPs) and spiking following brief depolarising current injections in the L2/3PCs. After 2 hours of pre-incubation with ketamine or propofol, the muscarine-induced PPs were altered in seemingly different ways: 3 μM propofol reduced the PPs and (significantly) spiking, whereas 20 μM ketamine seemed to enhance PPs and spiking (non-significantly). Brief wash-in of these drug concentrations failed to induce such effects, probably due to insufficient equilibration by diffusion in the slices. In contrast, pre-incubation with a high dose (100 μM) of ketamine suppressed the PPs and spiking. We discuss whether the apparently different effects on PPs may possibly be related to contrasting clinical effects: ketamine causing atypical anaesthesia with vivid, "psychedelic" dreaming while propofol causes less dreaming.

Indexed as

KetaminePropofolPyramidal CellsAction PotentialsAnesthetics, IntravenousAnimalsMaleMuscarineNeocortexPatch-Clamp TechniquesPrefrontal CortexRatsAnesthetics, IntravenousKetamineMuscarinePropofol

Identifiers

PMID39746093
PMCPMC11695037

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Registered trials

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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.