Evidence map›Paper›PMID 35290792›Full record

ArticleNeuron2022

A weakened recurrent circuit in the hippocampus of Rett syndrome mice disrupts long-term memory representations.

Lingjie He, Matthew S Caudill, Junzhan Jing, Wei Wang, Yaling Sun, Jianrong Tang, Xiaolong Jiang, Huda Y Zoghbi

Open access · greenAbstract read
In one paragraph

Article in Neuron, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
5.4field-weighted citation impact, top 4% 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

16 citing papers in PubMed, 30 citations in OpenAlex.

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  10. Use-Dependent, Untapped Dual Kinase Signaling Localized in Brain Learning Circuitry.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

Lingjie HeDepartment of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX, USA; Jan and Dan Duncan Neurological Research Institute at Texas Children's Hospital, Houston, TX, USA; Howard Hughes Medical Institute, Baylor College of Medicine, Houston, TX, USA.
Matthew S CaudillJan and Dan Duncan Neurological Research Institute at Texas Children's Hospital, Houston, TX, USA; Department of Neuroscience, Baylor College of Medicine, Houston, TX, USA.
Junzhan JingJan and Dan Duncan Neurological Research Institute at Texas Children's Hospital, Houston, TX, USA; Department of Neuroscience, Baylor College of Medicine, Houston, TX, USA.
Wei WangDepartment of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX, USA; Jan and Dan Duncan Neurological Research Institute at Texas Children's Hospital, Houston, TX, USA.
Yaling SunJan and Dan Duncan Neurological Research Institute at Texas Children's Hospital, Houston, TX, USA; Howard Hughes Medical Institute, Baylor College of Medicine, Houston, TX, USA.
Jianrong TangJan and Dan Duncan Neurological Research Institute at Texas Children's Hospital, Houston, TX, USA; Department of Pediatrics, Baylor College of Medicine, Houston, TX, USA.
Xiaolong JiangJan and Dan Duncan Neurological Research Institute at Texas Children's Hospital, Houston, TX, USA; Department of Neuroscience, Baylor College of Medicine, Houston, TX, USA.
Huda Y ZoghbiDepartment of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX, USA; Jan and Dan Duncan Neurological Research Institute at Texas Children's Hospital, Houston, TX, USA; Department of Neuroscience, Baylor College of Medicine, Houston, TX, USA; Department of Pediatrics, Baylor College of Medicine, Houston, TX, USA; Department of Neurology, Baylor College of Medicine, Houston, TX, USA; Howard Hughes Medical Institute, Baylor College of Medicine, Houston, TX, USA. Electronic address: hzoghbi@bcm.edu.
Baylor College of Medicine · USHoward Hughes Medical Institute · USTexas Medical Center · US

Funding

Preclinical and Clincial OutcomesP50HD103555 · NICHD · BAYLOR COLLEGE OF MEDICINE · PI Sandesh Chakravarthy Sreenath Nagamani, David Loren Nelson · 2020 to 2026
$9.9M
MOLECULAR PATHOGENESIS STUDIES OF RETT SYNDROMER01NS057819 · NINDS · BAYLOR COLLEGE OF MEDICINE · PI ZOGHBI, HUDA Y · 2006 to 2025
$7.5M
Studying the effects and mechanisms of deep brain stimulation in Rett syndrome miceR01NS100738 · NINDS · BAYLOR COLLEGE OF MEDICINE · PI Jianrong Tang · 2018 to 2026
$3.3M
Development of aberrant cortical interneuron circuitry in genetic mouse models of absence epilepsyR01NS110767 · NINDS · BAYLOR COLLEGE OF MEDICINE · PI JIANG, XIAOLONG, NOEBELS, JEFFREY · 2020 to 2024
$2.2M
Deciphering the building blocks of the macaque prefrontal cortical microcircuitR01MH120404 · NIMH · BAYLOR COLLEGE OF MEDICINE · PI JIANG, XIAOLONG · 2019 to 2023
$2.0M
Deciphering the transcriptomic signatures, physiology, and connectivity of the specialized morphotypes in macaque insular cortexR01MH122169 · NIMH · BAYLOR COLLEGE OF MEDICINE · PI JIANG, XIAOLONG · 2020 to 2024
$1.2M
Deep brain stimulation in Rett syndrome mice: cognitive benefits and their mechanismsR56NS100738 · NINDS · BAYLOR COLLEGE OF MEDICINE · PI TANG, JIANRONG · 2017 to 2017
$338k
Howard Hughes Medical InstituteNICHD NIH HHS P50 HD103555NIMH NIH HHS R01 MH120404NIMH NIH HHS R01 MH122169NINDS NIH HHS R01 NS057819NINDS NIH HHS R01 NS100738NINDS NIH HHS R01 NS110767NINDS NIH HHS R56 NS100738
6 · The paper itself

Abstract

Successful recall of a contextual memory requires reactivating ensembles of hippocampal cells that were allocated during memory formation. Altering the ratio of excitation-to-inhibition (E/I) during memory retrieval can bias cell participation in an ensemble and hinder memory recall. In the case of Rett syndrome (RTT), a neurological disorder with severe learning and memory deficits, the E/I balance is altered, but the source of this imbalance is unknown. Using in vivo imaging during an associative memory task, we show that during long-term memory retrieval, RTT CA1 cells poorly distinguish mnemonic context and form larger ensembles than wild-type mouse cells. Simultaneous multiple whole-cell recordings revealed that mutant somatostatin expressing interneurons (SOM) are poorly recruited by CA1 pyramidal cells and are less active during long-term memory retrieval in vivo. Chemogenetic manipulation revealed that reduced SOM activity underlies poor long-term memory recall. Our findings reveal a disrupted recurrent CA1 circuit contributing to RTT memory impairment.

Indexed as

Rett SyndromeAnimalsHippocampusInterneuronsMemory DisordersMemory, Long-TermMicePyramidal CellsE/I balanceinhibitionmemory retrievalneural ensembleRett syndromesomatostatin cells

Identifiers

PMID35290792
PMCPMC9930308
OpenAlexW4220856627

What OpenQuestion holds

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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.