Evidence map›Paper›PMID 42603171›Full record

ArticlePsychopharmacology2026

Chronic nicotine vapor-induced enhancement of ethanol drinking-in-the-dark is associated with reduced medial prefrontal cortical activity.

Timothy G Freels, Jennifer Li, Rebecca G Pavchinskiy, Rubing Zhao-Shea, Gilles E Martin, Andrew R Tapper

Abstract read
PubMed Publisher
In one paragraph

Article in Psychopharmacology, 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
–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

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

6 authors.

Timothy G FreelsBrudnick Neuropsychiatric Research Institute, Department of Neurobiology, University of Massachusetts Chan Medical School, Worcester, MA, USA. Timothy.Freels@umassmed.edu.ORCID https://orcid.org/0000-0002-0818-1526
Jennifer LiBrudnick Neuropsychiatric Research Institute, Department of Neurobiology, University of Massachusetts Chan Medical School, Worcester, MA, USA.
Rebecca G PavchinskiyBrudnick Neuropsychiatric Research Institute, Department of Neurobiology, University of Massachusetts Chan Medical School, Worcester, MA, USA.
Rubing Zhao-SheaBrudnick Neuropsychiatric Research Institute, Department of Neurobiology, University of Massachusetts Chan Medical School, Worcester, MA, USA.
Gilles E MartinBrudnick Neuropsychiatric Research Institute, Department of Neurobiology, University of Massachusetts Chan Medical School, Worcester, MA, USA.
Andrew R TapperBrudnick Neuropsychiatric Research Institute, Department of Neurobiology, University of Massachusetts Chan Medical School, Worcester, MA, USA.

Funding

NIDA NIH HHS DA041482NIMH NIH HHS MH137986
6 · The paper itself

Abstract

rationaleNicotine vaping is associated with increased alcohol use, including binge drinking, yet the neurobehavioral mechanisms underlying nicotine-alcohol interactions remain poorly understood due to limited translational preclinical models capturing intrapulmonary nicotine exposure effects on binge-like ethanol intake.

objectivesWe establish a mouse model combining nicotine vapor exposure (NVE) with drinking-in-the-dark (DID) to examine effects on binge-like ethanol (EtOH) consumption and determine whether these effects are associated with medial prefrontal cortex (mPFC) activity and nicotinic acetylcholine receptor (nAChR) signaling.

methodsMale and female mice were passively exposed to nicotine or vehicle vapor prior to 2-h and 4-h EtOH DID across repeated cycles. EtOH intake, blood ethanol concentrations (BECs), and control solution consumption were measured. Neuronal activation in prelimbic (PrL) and medial orbitofrontal cortex (mOFC) was assessed using c-Fos immunofluorescence. Mecamylamine was used to evaluate nAChR involvement.

resultsNVE produced physiologically relevant nicotine exposure and selectively increased EtOH consumption during 2-h and 4-h DID sessions without altering control solution intake. NVE also elevated BECs, which were positively correlated with EtOH consumption. Following DID, NVE was associated with reduced mPFC activity in PrL and mOFC; however, EtOH consumption was inversely correlated specifically with mOFC activity. nAChR blockade attenuated NVE-induced increases in EtOH consumption during 2-h DID only.

conclusionsPassive nicotine vapor exposure enhances binge-like EtOH intake and is associated with reduced mPFC engagement, particularly within mOFC, suggesting a mechanism underlying nicotine-alcohol interactions. These effects are partly mediated by nAChRs, identifying mPFC nAChRs as potential therapeutic targets for nicotine-alcohol polysubstance use.

Indexed as

Drinking-in-the-darkEthanolMale and female miceNicotine vaporNicotinic acetylcholinergic receptorOrbitofrontal cortexPolysubstance usePrefrontal cortex

Identifiers

PMID42603171

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.