Evidence map›Paper›PMID 25673857›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2015

Sensory deprivation disrupts homeostatic regeneration of newly generated olfactory sensory neurons after injury in adult mice.

Shu Kikuta, Takashi Sakamoto, Shin Nagayama, Kaori Kanaya, Makoto Kinoshita, Kenji Kondo, Koichi Tsunoda, Kensaku Mori, Tatsuya Yamasoba

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

40 citing papers in PubMed, 82 citations in OpenAlex.

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  6. A new surgical technique to increase airflow in the olfactory cleft: superior turbinate lateralization procedure.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2024
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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

9 authors at 2 institutions in 1 country.

Shu KikutaDepartment of Otolaryngology and Department of Physiology, Graduate School of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan, sh-kiku@m.u-tokyo.ac.jp.
Takashi SakamotoDepartment of Otolaryngology and.
Shin NagayamaDepartment of Neurobiology and Anatomy, University of Texas Medical School at Houston, Houston, Texas 77030, and.
Kaori KanayaDepartment of Otolaryngology and.
Makoto KinoshitaDepartment of Otolaryngology and.ORCID http://orcid.org/0000-0001-5447-7232
Kenji KondoDepartment of Otolaryngology and.
Koichi TsunodaDepartment of Artificial Organs and Medical Device Creation, National Institute of Sensory Organs, Tokyo Medical Center, National Hospital Organization, Meguro-ku, Tokyo 152-8902, Japan.
Kensaku MoriDepartment of Physiology, Graduate School of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan.
Tatsuya YamasobaDepartment of Otolaryngology and.
The University of Tokyo · JPTokyo Medical Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although it is well known that injury induces the generation of a substantial number of new olfactory sensory neurons (OSNs) in the adult olfactory epithelium (OE), it is not well understood whether olfactory sensory input influences the survival and maturation of these injury-induced OSNs in adults. Here, we investigated whether olfactory sensory deprivation affected the dynamic incorporation of newly generated OSNs 3, 7, 14, and 28 d after injury in adult mice. Mice were unilaterally deprived of olfactory sensory input by inserting a silicone tube into their nostrils. Methimazole, an olfactotoxic drug, was also injected intraperitoneally to bilaterally ablate OSNs. The OE was restored to its preinjury condition with new OSNs by day 28. No significant differences in the numbers of olfactory marker protein-positive mature OSNs or apoptotic OSNs were observed between the deprived and nondeprived sides 0-7 d after injury. However, between days 7 and 28, the sensory-deprived side showed markedly fewer OSNs and mature OSNs, but more apoptotic OSNs, than the nondeprived side. Intrinsic functional imaging of the dorsal surface of the olfactory bulb at day 28 revealed that responses to odor stimulation were weaker in the deprived side compared with those in the nondeprived side. Furthermore, prevention of cell death in new neurons 7-14 d after injury promoted the recovery of the OE. These results indicate that, in the adult OE, sensory deprivation disrupts compensatory OSN regeneration after injury and that newly generated OSNs have a critical time window for sensory-input-dependent survival 7-14 d after injury.

Indexed as

AnimalsAntithyroid AgentsApoptosisCaspase InhibitorsCell ProliferationCell SurvivalHomeostasisMaleMethimazoleMiceMice, Inbred C57BLNerve RegenerationOlfactory MucosaOlfactory Receptor NeuronsSensory DeprivationAntithyroid AgentsCaspase InhibitorsMethimazoleapoptosishomeostatic regenerationolfactory epitheliumolfactory sensory neuronsensory deprivation

Identifiers

PMID25673857
PMCPMC6605607
OpenAlexW2077206003

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.