Evidence map›Paper›PMID 40632689›Full record

ArticlePloS one2025

Pain-stimulated ultrasound vocalizations and their impact on pain response in mice.

Satoka Kasai, Saki Ukai, Junpei Kuroda, Tsugumi Yamauchi, Daisuke Yamada, Akiyoshi Saitoh, Satoshi Iriyama, Masashi Suzuki, Kazuki Arita, Yoshio Nakano and 2 more

Abstract read
In one paragraph

Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

12 authors.

Satoka KasaiLaboratory of Pharmacology and Therapeutics, Department of Pharmacy, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Katsushika-ku, Tokyo, Japan.ORCID https://orcid.org/0009-0000-3153-6869
Saki UkaiLaboratory of Pharmacology and Therapeutics, Department of Pharmacy, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Katsushika-ku, Tokyo, Japan.
Junpei KurodaLaboratory of Pharmacology and Therapeutics, Department of Pharmacy, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Katsushika-ku, Tokyo, Japan.
Tsugumi YamauchiLaboratory of Pharmacology, Department of Pharmacy, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Katsushika-ku, Tokyo, Japan.
Daisuke YamadaLaboratory of Pharmacology, Department of Pharmacy, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Katsushika-ku, Tokyo, Japan.
Akiyoshi SaitohLaboratory of Pharmacology, Department of Pharmacy, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Katsushika-ku, Tokyo, Japan.
Satoshi IriyamaLaboratory of Quantum information dynamics, Department of Information Sciences, Faculty of Science and Technology, Tokyo University of Science, Noda, Chiba, Japan.
Masashi SuzukiFUJIMIC, Inc., Tokyo, Japan.
Kazuki AritaLaboratory of Bioinformatics, Department of Pharmacy, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Katsushika-ku, Tokyo, Japan.
Yoshio NakanoLaboratory of Bioinformatics, Department of Pharmacy, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Katsushika-ku, Tokyo, Japan.
Satoru MiyazakiLaboratory of Bioinformatics, Department of Pharmacy, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Katsushika-ku, Tokyo, Japan.
Kazumi YoshizawaLaboratory of Pharmacology and Therapeutics, Department of Pharmacy, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Katsushika-ku, Tokyo, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pain is a complex phenomenon encompassing both the physiological and psychological aspects of sensation and emotion, respectively. In recent years, pain has been clarified to arise even without direct injury, with emotional transmission as a cause. However, the specific mechanisms behind emotional transmission are still not well understood. In this study, sounds in the ultrasonic domain that were recorded during pain stimulation in mice were used as sound stress to examine the effects of psychological stress caused by exposure to ultrasound on tactile thresholds. We also examined the effects of psychological stress caused by the ultrasound on an inflammatory pain model of mice. The tactile threshold decreased the next and three days after sound stress exposure in mice. DNA microarray analysis of the mouse thalamus exposed to sound stress revealed increased expression of inflammation-related genes, Prostaglandin-endoperoxide synthase 2 and C-X-C motif chemokine ligand 1. Their respective inhibitors, loxoprofen and SB225002, significantly improved hyperalgesia induced by sound stress. When sound stress was applied to a mouse model of inflammatory pain in which pain thresholds were restored 14 days after complete Freund's adjuvant administration, prolonged pain and attenuated analgesic effects of loxoprofen were observed. These results suggest that sound stress not only induces inflammation in the brain that causes hyperalgesia but may also be partially responsible for exacerbating inflammatory pain, hence complicating treatment.

Indexed as

PainUltrasonic WavesVocalization, AnimalAnimalsCyclooxygenase 2Disease Models, AnimalHyperalgesiaInflammationMaleMiceMice, Inbred C57BLPain ThresholdStress, PsychologicalCyclooxygenase 2

Identifiers

PMID40632689
PMCPMC12240302

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.