Evidence map›Paper›PMID 37649698›Full record

ArticleiScience2023

P2X7 purinergic receptor modulates dentate gyrus excitatory neurotransmission and alleviates schizophrenia-like symptoms in mouse.

Lumei Huang, Paula Mut-Arbona, Bernadett Varga, Bibiana Török, János Brunner, Antonia Arszovszki, András Iring, Máté Kisfali, E Sylvester Vizi, Beáta Sperlágh

Open access · goldAbstract read
In one paragraph

Article in iScience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

2 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
  2. Review
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

10 authors at 2 institutions in 1 country.

Lumei HuangLaboratory of Molecular Pharmacology, Institute of Experimental Medicine, 1083 Budapest, Hungary.
Paula Mut-ArbonaLaboratory of Molecular Pharmacology, Institute of Experimental Medicine, 1083 Budapest, Hungary.
Bernadett VargaLaboratory of Molecular Pharmacology, Institute of Experimental Medicine, 1083 Budapest, Hungary.
Bibiana TörökLaboratory of Molecular Pharmacology, Institute of Experimental Medicine, 1083 Budapest, Hungary.
János BrunnerLaboratory of Cellular Neuropharmacology, Institute of Experimental Medicine, 1083 Budapest, Hungary.
Antonia ArszovszkiLaboratory of Cellular Neuropharmacology, Institute of Experimental Medicine, 1083 Budapest, Hungary.
András IringLaboratory of Molecular Pharmacology, Institute of Experimental Medicine, 1083 Budapest, Hungary.
Máté KisfaliLaboratory of Molecular Neurobiology, Institute of Experimental Medicine, 1083 Budapest, Hungary.
E Sylvester ViziLaboratory of Molecular Pharmacology, Institute of Experimental Medicine, 1083 Budapest, Hungary.
Beáta SperlághLaboratory of Molecular Pharmacology, Institute of Experimental Medicine, 1083 Budapest, Hungary.
HUN-REN Institute of Experimental Medicine · HUSemmelweis University · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

ATP-gated P2X7 receptors (P2X7Rs) play a crucial role in brain disorders. However, how they affect normal and pathological synaptic transmission is still largely unclear. Here, by using whole-cell patch-clamp technique to record AMPA- and NMDA receptor-mediated excitatory postsynaptic currents (s/mEPSCs) in dentate gyrus granule cells (DG GCs), we revealed a modulation by P2X7Rs of presynaptic sites, especially originated from entorhinal cortex (EC)-GC path but not the mossy cell (MC)-GC path. The involvement of P2X7Rs was confirmed using a pharmacological approach. Additionally, the acute activation of P2X7Rs directly elevated calcium influx from EC-GC terminals. In postnatal phencyclidine (PCP)-induced mouse model of schizophrenia, we observed that P2X7R deficiency restored the EC-GC synapse alteration and alleviated PCP-induced symptoms. To summarize, P2X7Rs participate in the modulation of GC excitatory neurotransmission in the DG via EC-GC pathway, contributing to pathological alterations of neuronal functions leading to neurodevelopmental disorders.

Indexed as

Behavioral neuroscienceBiological sciencesNatural sciencesNeurosciencePharmacologyPhysiology

Identifiers

PMID37649698
PMCPMC10462828
OpenAlexW4385617645

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.