Evidence map›Paper›PMID 41042799›Full record

ArticlePLoS biology2025

Nicotine induces abnormal motor coupling through sensitization of a mechanosensory circuit in Caenorhabditis elegans.

Yuting Liu, Leiru Huang, Ruipeng Wang, Fukang Qi, Yiwen Liu, Qingyuan Chen, Morgane Mialon, Lili Chen, Berangere Pinan-Lucarre, Shangbang Gao

Abstract read
In one paragraph

Article in PLoS biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Advances in drug addiction research usingFrontiers in cell and developmental biology · 2026
    Review
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

10 authors.

Yuting LiuKey Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, China.
Leiru HuangKey Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, China.
Ruipeng WangKey Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, China.
Fukang QiKey Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, China.
Yiwen LiuKey Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, China.
Qingyuan ChenKey Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, China.
Morgane MialonMelis, Universite Claude Bernard Lyon 1, CNRS UMR5284, INSERM U1314, Institut NeuroMyoGene-Faculte de Medecine et de Pharmacie, Lyon, France.
Lili ChenKey Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, China.
Berangere Pinan-LucarreMelis, Universite Claude Bernard Lyon 1, CNRS UMR5284, INSERM U1314, Institut NeuroMyoGene-Faculte de Medecine et de Pharmacie, Lyon, France.
Shangbang GaoKey Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, China.ORCID 0000-0001-5431-4628

Funding

Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Ann E. Rougvie · 2012 to 2026
$7.5M
NIH HHS P40 OD010440
6 · The paper itself

Abstract

Nicotine exposure elicits diverse behavioral changes, yet the underlying neural pathways and molecular mechanisms remain incompletely understood. Here, we demonstrate that chronic nicotine exposure markedly increases both the initiation and duration of reversals in Caenorhabditis elegans. Strikingly, these reversals were tightly coupled with the rhythmic body contractions of the defecation motor program (DMP). Through pharmacological, genetic, in situ electrophysiological, and calcium imaging analyses, we show that nicotine enhances the activity of the AVA interneuron via selective upregulation of ACR-16, a nicotinic ACh receptor critical for nicotine-induced motor coupling. Ablation of touch receptor neurons (TRNs) or inhibition of TRNs-mediated mechanosensation completely abolished this coupling. Furthermore, optogenetic activation of TRNs in nicotine-treated animals evoked stronger AVA depolarization, and nicotine amplified gentle touch-evoked reversals. Together, these findings reveal a potential interoceptive effect of nicotine mediated by sensitization of the TRNs-AVA mechanosensory pathway, providing new insight into the neural and molecular basis of nicotine's modulation of sensory-motor coupling.

Indexed as

Caenorhabditis elegansMechanotransduction, CellularNicotineAnimalsCaenorhabditis elegans ProteinsDefecationInterneuronsNicotinic AgonistsOptogeneticsReceptors, NicotinicSensory Receptor CellsCaenorhabditis elegans ProteinsNicotineNicotinic AgonistsReceptors, Nicotinic

Identifiers

PMID41042799
PMCPMC12507281

What OpenQuestion holds

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LicenceCC BY
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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.