Evidence map›Paper›PMID 34980635›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2022

Hyper-Rigid Phasic Organization of Hippocampal Activity But Normal Spatial Properties of CA1 Place Cells in the Ts65Dn Mouse Model of Down Syndrome.

Robert G K Munn, Aimée Freeburn, David P Finn, H Craig Heller

Abstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
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

4 authors.

Robert G K MunnDepartment of Anatomy, University of Otago, Dunedin, New Zealand, 9016 robert.munn@otago.ac.nz.
Aimée FreeburnDiscipline of Pharmacology and Therapeutics, National University of Ireland, Galway, Galway, Ireland, H91 TK33.
David P FinnDiscipline of Pharmacology and Therapeutics, National University of Ireland, Galway, Galway, Ireland, H91 TK33.
H Craig HellerDepartment of Biology, Stanford University, Stanford, CA 94305.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Down syndrome (DS) in humans is caused by trisomy of chromosome 21 and is marked by prominent difficulties in learning and memory. Decades of research have demonstrated that the hippocampus is a key structure in learning and memory, and recent work with mouse models of DS has suggested differences in hippocampal activity that may be the substrate of these differences. One of the primary functional differences in DS is thought to be an excess of GABAergic innervation from medial septum to the hippocampus. In these experiments, we probe in detail the activity of region CA1 of the hippocampus using

Indexed as

Down SyndromePlace CellsAnimalsDisease Models, AnimalGamma RhythmHippocampusMaleMiceDown syndromehippocampuslearning and memoryplace celltheta rhythmTs65Dn

Identifiers

PMID34980635
PMCPMC8883859

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.