Evidence map›Paper›PMID 26717882›Full record

ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2016

Activin Controls Ethanol Potentiation of Inhibitory Synaptic Transmission Through GABAA Receptors and Concomitant Behavioral Sedation.

Fang Zheng, Anne Puppel, Sabine E Huber, Andrea S Link, Volker Eulenburg, Johannes F van Brederode, Christian P Müller, Christian Alzheimer

Open access · bronzeAbstract read
In one paragraph

Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2016. 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
1.4field-weighted citation impact, top 21% 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

14 citing papers in PubMed, 28 citations in OpenAlex.

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  6. Pyridoxal kinase inhibition by artemisinins down-regulates inhibitory neurotransmission.Proceedings of the National Academy of Sciences of the United States of America · 2020
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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

8 authors at 2 institutions in 1 country.

Fang ZhengInstitute of Physiology and Pathophysiology, Friedrich-Alexander-Universität, Erlangen-Nürnberg, Erlangen, Germany.
Anne PuppelInstitute of Physiology and Pathophysiology, Friedrich-Alexander-Universität, Erlangen-Nürnberg, Erlangen, Germany.
Sabine E HuberDepartment of Psychiatry and Psychotherapy, Universitätsklinikum Erlangen, Erlangen, Germany.
Andrea S LinkInstitute of Physiology and Pathophysiology, Friedrich-Alexander-Universität, Erlangen-Nürnberg, Erlangen, Germany.
Volker EulenburgInstitute of Biochemistry, Friedrich-Alexander-Universität, Erlangen-Nürnberg, Erlangen, Germany.
Johannes F van BrederodeInstitute of Physiology and Pathophysiology, Friedrich-Alexander-Universität, Erlangen-Nürnberg, Erlangen, Germany.
Christian P MüllerDepartment of Psychiatry and Psychotherapy, Universitätsklinikum Erlangen, Erlangen, Germany.
Christian AlzheimerInstitute of Physiology and Pathophysiology, Friedrich-Alexander-Universität, Erlangen-Nürnberg, Erlangen, Germany.
Friedrich-Alexander-Universität Erlangen-Nürnberg · DEUniversitätsklinikum Erlangen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Activin, a member of the transforming growth factor-β family, exerts multiple functions in the nervous system. Originally identified as a neurotrophic and -protective agent, increasing evidence implicates activin also in the regulation of glutamatergic and GABAergic neurotransmission in brain regions associated with cognitive and affective functions. To explore how activin impacts on ethanol potentiation of GABA synapses and related behavioral paradigms, we used an established transgenic model of disrupted activin receptor signaling, in which mice express a dominant-negative activin receptor IB mutant (dnActRIB) under the control of the CaMKIIα promoter. Comparison of GABAA receptor currents in hippocampal neurons from dnActRIB mice and wild-type mice showed that all concentrations of ethanol tested (30-150 mM) produced much stronger potentiation of phasic inhibition in the mutant preparation. In dentate granule cells of dnActRIB mice, tonic GABA inhibition was more pronounced than in wild-type neurons, but remained insensitive to low ethanol (30 mM) in both preparations. The heightened ethanol sensitivity of phasic inhibition in mutant hippocampi resulted from both pre- and postsynaptic mechanisms, the latter probably involving PKCɛ. At the behavioral level, ethanol produced significantly stronger sedation in dnActRIB mice than in wild-type mice, but did not affect consumption of ethanol or escalation after withdrawal. We link the abnormal narcotic response of dnActRIB mice to ethanol to the excessive potentiation of inhibitory neurotransmission. Our study suggests that activin counteracts oversedation from ethanol by curtailing its augmenting effect at GABA synapses.

Indexed as

Activin ReceptorsActivinsAnimalsBehavior, AnimalEthanolHippocampusHypnotics and SedativesInhibitory Postsynaptic PotentialsMiceMice, TransgenicNeural InhibitionProtein Kinase C-epsilonPyramidal CellsReceptors, GABA-ARewardActivin ReceptorsActivinsEthanolHypnotics and SedativesProtein Kinase C-epsilonReceptors, GABA-A

Identifiers

PMID26717882
PMCPMC4908639
OpenAlexW2265025055

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.