Evidence map›Paper›PMID 32111927›Full record

ArticleScientific reports2020

Layer-specific sensory processing impairment in the primary somatosensory cortex after motor cortex infarction.

Atsushi Fukui, Hironobu Osaki, Yoshifumi Ueta, Kenta Kobayashi, Yoshihiro Muragaki, Takakazu Kawamata, Mariko Miyata

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 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

17 citing papers in PubMed, 25 citations in OpenAlex.

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  13. Post-Ischemic Reorganization of Sensory Responses in Cerebral Cortex.bioRxiv : the preprint server for biology · 2023
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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

7 authors at 2 institutions in 1 country.

Atsushi Fukui *Faculty of Advanced Techno-Surgery, Institute of Advanced Biomedical Engineering and Science, Tokyo Women's Medical University, Tokyo, Japan.
Hironobu Osaki *Division of Neurophysiology, Department of Physiology, School of Medicine, Tokyo Women's Medical University, Tokyo, Japan. osaki.hironobu@twmu.ac.jp.ORCID http://orcid.org/0000-0001-9780-0810
Yoshifumi UetaDivision of Neurophysiology, Department of Physiology, School of Medicine, Tokyo Women's Medical University, Tokyo, Japan.ORCID http://orcid.org/0000-0002-3073-9899
Kenta KobayashiSection of Viral Vector Development, National Institute for Physiological Sciences, Okazaki, Japan.
Yoshihiro MuragakiFaculty of Advanced Techno-Surgery, Institute of Advanced Biomedical Engineering and Science, Tokyo Women's Medical University, Tokyo, Japan.
Takakazu KawamataDepartment of Neurosurgery, Tokyo Women's Medical University, Tokyo, Japan.
Mariko MiyataDivision of Neurophysiology, Department of Physiology, School of Medicine, Tokyo Women's Medical University, Tokyo, Japan. mmiyata@twmu.ac.jp.ORCID http://orcid.org/0000-0001-5688-654X
Tokyo Women's Medical University · JPThe Graduate University for Advanced Studies, SOKENDAI · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Primary motor cortex (M1) infarctions sometimes cause sensory impairment. Because sensory signals play a vital role in motor control, sensory impairment compromises the recovery and rehabilitation of motor disability. However, the neural mechanism of the sensory impairment is poorly understood. We show that sensory processing in mouse primary somatosensory cortex (S1) was impaired in the acute phase of M1 infarctions and recovered in a layer-specific manner in the subacute phase. This layer-dependent recovery process and the anatomical connection pattern from M1 to S1 suggested that functional connectivity from M1 to S1 plays a key role in the sensory processing impairment. A simulation study demonstrated that the loss of inhibition from M1 to S1 in the acute phase of M1 infarctions could impair sensory processing in S1, and compensation for the inhibition could recover the temporal coding. Consistently, the optogenetic activation of M1 suppressed the sustained response in S1. Taken together, we revealed how focal stroke in M1 alters the cortical network activity of sensory processing, in which inhibitory input from M1 to S1 may be involved.

Indexed as

SensationAnimalsBrain InfarctionMaleMiceOptogeneticsSomatosensory CortexStroke

Identifiers

PMID32111927
PMCPMC7048762
OpenAlexW3009731615

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.