Evidence map›Paper›PMID 26531194›Full record

ArticleActa neuropathologica communications2015

Muscarinic M1 receptors modulate endotoxemia-induced loss of synaptic plasticity.

Aleksandar R Zivkovic, Oliver Sedlaczek, Rebecca von Haken, Karsten Schmidt, Thorsten Brenner, Markus A Weigand, Hilmar Bading, C Peter Bengtson, Stefan Hofer

Abstract read
In one paragraph

Article in Acta neuropathologica communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

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  5. N-acetyltransferase 10 mediates cognitive dysfunction through the acetylation of GABAProceedings of the National Academy of Sciences of the United States of America · 2024
    Article
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  11. Article
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  13. Observational
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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

9 authors.

Aleksandar R ZivkovicDepartment of Anesthesiology, Heidelberg University Hospital, Im Neuenheimer Feld 110, 69120, Heidelberg, Germany. aleksandar.zivkovic@med.uni-heidelberg.de.
Oliver SedlaczekDepartment of Radiology, Heidelberg University Hospital, Im Neuenheimer Feld 110, 69120, Heidelberg, Germany.
Rebecca von HakenDepartment of Anesthesiology, Heidelberg University Hospital, Im Neuenheimer Feld 110, 69120, Heidelberg, Germany.
Karsten SchmidtDepartment of Anesthesiology, Heidelberg University Hospital, Im Neuenheimer Feld 110, 69120, Heidelberg, Germany.
Thorsten BrennerDepartment of Anesthesiology, Heidelberg University Hospital, Im Neuenheimer Feld 110, 69120, Heidelberg, Germany.
Markus A WeigandDepartment of Anesthesiology, Heidelberg University Hospital, Im Neuenheimer Feld 110, 69120, Heidelberg, Germany.
Hilmar BadingNeurobiology, Interdisciplinary Centre for Neurosciences (IZN), University of Heidelberg, Im Neuenheimer Feld 364, 69120, Heidelberg, Germany.
C Peter BengtsonNeurobiology, Interdisciplinary Centre for Neurosciences (IZN), University of Heidelberg, Im Neuenheimer Feld 364, 69120, Heidelberg, Germany. bengtson@nbio.uniheidelberg.de.
Stefan HoferDepartment of Anesthesiology, Heidelberg University Hospital, Im Neuenheimer Feld 110, 69120, Heidelberg, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Septic encephalopathy is associated with rapid deterioration of cortical functions. Using magnetic resonance imaging (MRI) we detected functional abnormalities in the hippocampal formation of patients with septic delirium. Hippocampal dysfunction was further investigated in an animal model for sepsis using lipopolysaccharide (LPS) injections to induce endotoxemia in rats, followed by electrophysiological recordings in brain slices. Endotoxemia induced a deficit in long term potentiation which was completely reversed by apamin, a blocker of small conductance calcium-activated potassium (SK) channels, and partly restored by treatment with physostigmine (eserine), an acetylcholinesterase inhibitor, or TBPB, a selective M1 muscarinic acetylcholine receptor agonist. These results suggest a novel role for SK channels in the etiology of endotoxemia and explain why boosting cholinergic function restores deficits in synaptic plasticity. Drugs which enhance cholinergic or M1 activity in the brain may prove beneficial in treatment of septic delirium in the intensive care unit.

Indexed as

Analysis of VarianceAnimalsApaminArea Under CurveBiophysicsCholinergic AgentsDiffusion Magnetic Resonance ImagingDisease Models, AnimalElectric StimulationHippocampusIn Vitro TechniquesLipopolysaccharidesLong-Term PotentiationNeuronal PlasticityNeuronsPatch-Clamp TechniquesApaminCholinergic AgentsLipopolysaccharidesReceptor, Muscarinic M1

Identifiers

PMID26531194
PMCPMC4632469

What OpenQuestion holds

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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.