Evidence map›Paper›PMID 41735225›Full record

ArticleNeurogastroenterology and motility2026

Possible Involvement of Descending Monoaminergic Pathways in Colorectal Dysmotility Using a Rat Model of Colitis.

Natsufu Yuki, Yuuno Hiroki, Tomoya Sawamura, Ayuna Mori, Kazuya Takashima, Yuuki Horii, Takahiko Shiina, Yasutake Shimizu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neurogastroenterology and motility, 2026. 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

8 authors.

Natsufu YukiDepartment of Basic Veterinary Science, Laboratory of Physiology, Joint Graduate School of Veterinary Sciences, Gifu University, Gifu, Japan.
Yuuno HirokiDepartment of Basic Veterinary Science, Laboratory of Physiology, Joint Department of Veterinary Medicine, Faculty of Applied Biological Sciences, Gifu University, Gifu, Japan.
Tomoya SawamuraDepartment of Basic Veterinary Science, Laboratory of Physiology, Joint Graduate School of Veterinary Sciences, Gifu University, Gifu, Japan.
Ayuna MoriDepartment of Basic Veterinary Science, Laboratory of Physiology, Joint Department of Veterinary Medicine, Faculty of Applied Biological Sciences, Gifu University, Gifu, Japan.
Kazuya TakashimaDepartment of Basic Veterinary Science, Laboratory of Physiology, Joint Department of Veterinary Medicine, Faculty of Applied Biological Sciences, Gifu University, Gifu, Japan.
Yuuki HoriiDepartment of Basic Veterinary Science, Laboratory of Physiology, Joint Department of Veterinary Medicine, Faculty of Applied Biological Sciences, Gifu University, Gifu, Japan.
Takahiko ShiinaDepartment of Basic Veterinary Science, Laboratory of Physiology, Joint Graduate School of Veterinary Sciences, Gifu University, Gifu, Japan.
Yasutake ShimizuDepartment of Basic Veterinary Science, Laboratory of Physiology, Joint Graduate School of Veterinary Sciences, Gifu University, Gifu, Japan.

Funding

Japan Society for the Promotion of Science 24KJ1212KAKENHI 23H00360
6 · The paper itself

Abstract

backgroundColonic inflammation is known to cause intestinal dysmotility. We examined the possible involvement of descending monoaminergic neurons projecting to the lumbosacral spinal cord in colorectal dysmotility using a rat model of colitis.

methodsColitis was induced in rats by intracolonic administration of 2,4,6-trinitrobenzenesulfonic acid. Motility in inflamed and noninflamed colorectal regions was assessed in vivo under anesthesia. KEY

resultsColonic inflammation suppressed colorectal motility responses to noxious stimulus applied on inflamed colonic regions. The suppressed responses recovered as inflammation improved. In a subset of rats with colitis, basal motility in noninflamed regions was significantly enhanced, and this was abolished by intrathecal administration of serotonergic and dopaminergic receptor antagonists to the lumbosacral spinal cord. In some rats, enhanced basal motility spontaneously subsided then returned to a hyperactive state. The re-enhanced basal motility was also suppressed by monoaminergic receptor antagonists, suggesting intermittent activity of the descending monoaminergic neurons. CONCLUSIONS AND INFERENCES: This study suggested that persistent noxious input from an inflamed colon activates descending monoaminergic neurons, leading to enhanced basal motility in noninflamed regions. Our findings provide important insights into the pathophysiology of inflammation-associated dysmotility.

Indexed as

Biogenic MonoaminesColitisColonGastrointestinal MotilityRectumAnimalsDisease Models, AnimalMaleRatsRats, Sprague-DawleySpinal CordTrinitrobenzenesulfonic AcidBiogenic MonoaminesTrinitrobenzenesulfonic Acidcentral nervous systemcolitisdopaminegastrointestinal motilityserotonintrinitrobenzenesulfonic acidTRPV1 cation channels

Identifiers

PMID41735225
PMCPMC12932259

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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.