Evidence map›Paper›PMID 39177808›Full record

ArticlePsychopharmacology2024

Evaluation of (S)-T1 and (S)-T2 ligands targeting α3β4 nAChR as potential nicotine addiction pharmacotherapy.

Saranda Nianpanich, Ratchanee Rodsiri, Ridho Islamie, Patanachai Limpikirati, Thanundorn Thanusuwannasak, Opa Vajragupta, Apinan Kanasuwan, Jiradanai Sarasamkan

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Article in Psychopharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited 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

8 authors.

Saranda NianpanichDepartment of Pharmacology and Physiology, Faculty of Pharmaceutical Sciences, Chulalongkorn University, Bangkok, 10330, Thailand.
Ratchanee RodsiriDepartment of Pharmacology and Physiology, Faculty of Pharmaceutical Sciences, Chulalongkorn University, Bangkok, 10330, Thailand.
Ridho IslamieDepartment of Clinical and Community Pharmacy, Faculty of Pharmacy, University of Surabaya, Surabaya, 60293, Indonesia.
Patanachai LimpikiratiDepartment of Food and Pharmaceutical Chemistry, Faculty of Pharmaceutical Sciences, Chulalongkorn University, Bangkok, 10330, Thailand.
Thanundorn ThanusuwannasakPharmaceutical Research Instrument Center, Faculty of Pharmaceutical Sciences, Chulalongkorn University, Bangkok, 10330, Thailand.
Opa VajraguptaMolecular Probes for Imaging Research Network, Faculty of Pharmaceutical Sciences, Chulalongkorn University, Bangkok, 10330, Thailand.
Apinan KanasuwanNational Cyclotron and PET Centre, Chulabhorn Hospital, Chulabhorn Royal Academy, Bangkok, 10210, Thailand.
Jiradanai SarasamkanDepartment of Radiology, Faculty of Medicine, Khon Kaen University, Khon Kaen, 40002, Thailand. jirasar@kku.ac.th.ORCID http://orcid.org/0000-0002-7484-0067

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesSubstance use disorders (SUDs) represent a significant global health concern, demanding the development of effective pharmacological treatments. To address this, an investigation was conducted to examine the anti-addictive properties of two compounds, (S)-T1 and (S)-T2, which specifically target the α3β4 nicotinic acetylcholine receptor (nAChR).

methodsThe effects of (S)-T1 and (S)-T2 on nicotine-induced conditioned place preference (CPP), locomotor activity and dopamine levels in particular brain regions associated to addiction were investigated and compared in male C57BL/6N mice.

resultsThe results demonstrate that neither (S)-T1 nor (S)-T2 induced place conditioning or conditioned place aversion (CPA), suggesting the absence of rewarding or aversive effects. Both compounds significantly attenuated nicotine-induced CPP, with (S)-T1 exhibiting a dose-dependent effect. Furthermore, the co-administration of (S)-T2 (10 mg/kg) with nicotine markedly reduced locomotor activity compared to nicotine treatment alone. Additionally, dopamine analysis revealed that nicotine increased dopamine levels in the nucleus accumbens (NAc) and dorsal striatum, whereas the co-administration of (S)-T1 (1, 3, and 10 mg/kg) and (S)-T2 (10 mg/kg) significantly decreased dopamine levels in these brain regions. No significant effects were observed in the prefrontal cortex (PFC).

conclusionsThese findings suggest that (S)-T1 and (S)-T2 hold promise for treating nicotine addiction by attenuating nicotine-induced CPP and modulating dopamine release in key reward-related brain regions. Further research is needed to gain insights into the underlying mechanisms behind their anti-addictive effects and substantiate their potential for treating nicotine addiction.

Indexed as

DopamineDose-Response Relationship, DrugMice, Inbred C57BLNicotineReceptors, NicotinicTobacco Use DisorderAnimalsBrainLigandsMaleMiceMotor ActivityNicotinic AgonistsNucleus AccumbensDopamineLigandsNicotineNicotinic Agonistsnicotinic receptor alpha3beta4Receptors, NicotinicNicotine addictionSUDsα3β4 nAChR

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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.