Evidence map›Paper›PMID 32724221›Full record

ArticleScientific reports2020

Cholesterol modulates presynaptic and postsynaptic properties of excitatory synaptic transmission.

Miloslav Korinek, Inmaculada M Gonzalez-Gonzalez, Tereza Smejkalova, Dragana Hajdukovic, Kristyna Skrenkova, Jan Krusek, Martin Horak, Ladislav Vyklicky

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
3.8field-weighted citation impact, top 5% 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

59 citing papers in PubMed, 80 citations in OpenAlex.

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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 3 institutions in 2 countries.

Miloslav KorinekDepartment of Cellular Neurophysiology, Institute of Physiology of the Czech Academy of Sciences, Videnska 1083, Prague, Czech Republic. miloslav.korinek@fgu.cas.cz.
Inmaculada M Gonzalez-GonzalezSchool of Pharmacy and Biomedical Sciences, University of Central Lancashire, Preston, UK.
Tereza SmejkalovaDepartment of Cellular Neurophysiology, Institute of Physiology of the Czech Academy of Sciences, Videnska 1083, Prague, Czech Republic.
Dragana HajdukovicDepartment of Cellular Neurophysiology, Institute of Physiology of the Czech Academy of Sciences, Videnska 1083, Prague, Czech Republic.
Kristyna SkrenkovaDepartment of Cellular Neurophysiology, Institute of Physiology of the Czech Academy of Sciences, Videnska 1083, Prague, Czech Republic.
Jan KrusekDepartment of Cellular Neurophysiology, Institute of Physiology of the Czech Academy of Sciences, Videnska 1083, Prague, Czech Republic.
Martin HorakDepartment of Cellular Neurophysiology, Institute of Physiology of the Czech Academy of Sciences, Videnska 1083, Prague, Czech Republic.
Ladislav VyklickyDepartment of Cellular Neurophysiology, Institute of Physiology of the Czech Academy of Sciences, Videnska 1083, Prague, Czech Republic.
Czech Academy of Sciences, Institute of Physiology · CZCzech Academy of Sciences · CZUniversity of Central Lancashire · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cholesterol is a structural component of cellular membranes particularly enriched in synapses but its role in synaptic transmission remains poorly understood. We used rat hippocampal cultures and their acute cholesterol depletion by methyl-β-cyclodextrin as a tool to describe the physiological role of cholesterol in glutamatergic synaptic transmission. Cholesterol proved to be a key molecule for the function of synapses as its depletion resulted in a significant reduction of both NMDA receptor (NMDAR) and AMPA/kainate receptor-mediated evoked excitatory postsynaptic currents (eEPSCs), by 94% and 72%, respectively. We identified two presynaptic and two postsynaptic steps of synaptic transmission which are modulated by cholesterol and explain together the above-mentioned reduction of eEPSCs. In the postsynapse, we show that physiological levels of cholesterol are important for maintaining the normal probability of opening of NMDARs and for keeping NMDARs localized in synapses. In the presynapse, our results favour the hypothesis of a role of cholesterol in the propagation of axonal action potentials. Finally, cholesterol is a negative modulator of spontaneous presynaptic glutamate release. Our study identifies cholesterol as an important endogenous regulator of synaptic transmission and provides insight into molecular mechanisms underlying the neurological manifestation of diseases associated with impaired cholesterol synthesis or decomposition.

Indexed as

Synaptic TransmissionAnimalsCerebral CortexCholesterolExcitatory Postsynaptic PotentialsGlutamic AcidHippocampusMaleNeuronsPresynaptic TerminalsRatsRats, WistarReceptors, AMPAReceptors, N-Methyl-D-AspartateSynapsesCholesterolGlutamic AcidReceptors, AMPAReceptors, N-Methyl-D-Aspartate

Identifiers

PMID32724221
PMCPMC7387334
OpenAlexW3045708843

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.