Evidence map›Paper›PMID 33214655›Full record

ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2021

Chronic α1-Na/K-ATPase inhibition reverses the elongation of the axon initial segment of the hippocampal CA1 pyramidal neurons in Angelman syndrome model mice.

Prudhvi Raj Rayi, Alexei Y Bagrov, Hanoch Kaphzan

Open access · bronzeAbstract read
In one paragraph

Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.7field-weighted citation impact, top 25% 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

4 citing papers in PubMed, 9 citations in OpenAlex.

  1. Involvement of the NaInternational journal of molecular sciences · 2024
    Article
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  3. Review
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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

3 authors at 2 institutions in 2 countries.

Prudhvi Raj RayiSagol Department of Neurobiology, The Integrated Brain and Behavior Research Center, University of Haifa, Haifa, 3498838, Israel.
Alexei Y BagrovSechenov Institute of Evolutionary Physiology and Biochemistry, 194223, St. Petersburg, Russian Federation.
Hanoch KaphzanSagol Department of Neurobiology, The Integrated Brain and Behavior Research Center, University of Haifa, Haifa, 3498838, Israel. hkaphzan@univ.haifa.ac.il.ORCID http://orcid.org/0000-0003-4935-358X
University of Haifa · ILInstitute of Evolutionary Physiology and Biochemistry · RU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Angelman syndrome (AS) is a neurodevelopmental disorder caused by the loss of function of the maternal UBE3A gene. The hippocampus is one of the most prominently affected brain regions in AS model mice, manifesting in severe hippocampal-dependent memory and plasticity deficits. Previous studies in AS mice reported an elongated axon initial segment (AIS) in pyramidal neurons (PNs) of the hippocampal CA1 region. These were the first reports in mammals to show AIS elongation in vivo. Correspondingly, this AIS elongation was linked to enhanced expression of the α1 subunit of Na

Indexed as

Angelman SyndromeAxon Initial SegmentAdenosine TriphosphatasesAnimalsCA1 Region, HippocampalHippocampusMicePyramidal CellsAdenosine Triphosphatases

Identifiers

PMID33214655
PMCPMC8027375
OpenAlexW3101173261

What OpenQuestion holds

Textmetadata
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.