Evidence map›Paper›PMID 41590740›Full record

ArticleMarine drugs2026

Hippocampal Metabolomics Reveal the Mechanism of α-Conotoxin [S9K]TxID Attenuating Nicotine Addiction.

Meiting Wang, Weifeng Xu, Huanbai Wang, Cheng Cui, Rongyan He, Xiaodan Li, Jinpeng Yu, J Michael McIntosh, Dongting Zhangsun, Sulan Luo

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Marine drugs, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Meiting WangGuangxi Key Laboratory of Special Biomedicine, School of Medicine, College of Life Science and Technology, Guangxi University, Nanning 530004, China.
Weifeng XuGuangxi Key Laboratory of Special Biomedicine, School of Medicine, College of Life Science and Technology, Guangxi University, Nanning 530004, China.
Huanbai WangGuangxi Key Laboratory of Special Biomedicine, School of Medicine, College of Life Science and Technology, Guangxi University, Nanning 530004, China.
Cheng CuiGuangxi Key Laboratory of Special Biomedicine, School of Medicine, College of Life Science and Technology, Guangxi University, Nanning 530004, China.
Rongyan HeGuangxi Key Laboratory of Special Biomedicine, School of Medicine, College of Life Science and Technology, Guangxi University, Nanning 530004, China.
Xiaodan LiKey Laboratory of Tropical Biological Resources of Ministry of Education, Hainan University, Haikou 570228, China.
Jinpeng YuGuangxi Key Laboratory of Special Biomedicine, School of Medicine, College of Life Science and Technology, Guangxi University, Nanning 530004, China.ORCID 0000-0002-4936-8637
J Michael McIntoshDepartments of Biology and Psychiatry, University of Utah, Salt Lake City, UT 84112, USA.
Dongting ZhangsunGuangxi Key Laboratory of Special Biomedicine, School of Medicine, College of Life Science and Technology, Guangxi University, Nanning 530004, China.
Sulan LuoGuangxi Key Laboratory of Special Biomedicine, School of Medicine, College of Life Science and Technology, Guangxi University, Nanning 530004, China.ORCID 0000-0002-9358-5970

Funding

Development and Application of Nicotinic Acetylcholine Receptor Targeted Peptides for Biomedical ResearchR35GM136430 · NIGMS · UNIVERSITY OF UTAH · PI MCINTOSH, J MICHAEL · 2020 to 2024
$2.3M
Dongting Zhangsun No. 82360698NIGMS NIH HHS R35 GM136430Sulan Luo 2022YFE0132700Sulan Luo 82320108019Sulan Luo GUIKE AA25069003Sulan Luo No. 2024GXNSFDA999003Sulan Luo No. 42376112
6 · The paper itself

Abstract

Nicotine is the main substance responsible for the development of tobacco addiction. The α3β4 nicotinic acetylcholine receptors (nAChRs) are a potential key target for mitigating nicotine reward. Preliminary studies in our laboratory suggest that α-conotoxin [S9K]TxID serves as a selective and potent antagonist targeting α3β4 nAChRs, which may be beneficial in addressing nicotine addiction. However, the mechanisms of [S9K]TxID treatment in nicotine addiction are still to be determined. This study aimed to identify the differential metabolic profiles of [S9K]TxID treatment in nicotine addiction using an untargeted metabolomic profiling method. As demonstrated by behavioral experiments, [S9K]TxID effectively attenuated nicotine-induced conditioned place preference (CPP) expression without exerting inhibitory effects on the central nervous system (CNS). The results of untargeted metabolomics revealed that eight metabolites were significantly altered after [S9K]TxID treatment, particularly phenylalanine. [S9K]TxID also attenuated nicotine-induced metabolic disorders by regulating phenylalanine, tyrosine and tryptophan biosynthesis. In conclusion, our findings suggest that [S9K]TxID could be a potential therapeutic compound for nicotine addiction.

Indexed as

ConotoxinsHippocampusNicotinic AntagonistsTobacco Use DisorderAnimalsMaleMetabolomicsNicotineRatsRats, Sprague-DawleyReceptors, NicotinicConotoxinsNicotineNicotinic Antagonistsnicotinic receptor alpha3beta4Receptors, NicotinicCPPmetabolomicsnicotine addictionα3β4 nAChRsα-conotoxin [S9K]TxID

Identifiers

PMID41590740
PMCPMC12842921

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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.