ArticleNeuropharmacology2025
Behavioral economics of polysubstance use: The role of orexin-1 receptors in nicotine-induced augmentation of synthetic opioid consumption.
Article in Neuropharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Nicotine and opioid use disorders are highly comorbid in clinical populations. Ongoing nicotine administration facilitates opioid consumption in both rodents and humans. Moreover, preclinical studies support that former exposure to nicotine solely during adolescence augments opioid consumption in adulthood similarly to acute nicotine administration. This suggests that developmental nicotine exposure persistently alters the neural substrates underlying motivation in a manner that resembles the acute pharmacological actions of nicotine. The orexin system mediates motivation to consume opioids in large part through signaling at orexin-1 receptors (ORX1Rs). Both developmental nicotine exposure and acute nicotine administration profoundly alter functioning of the orexin system which may mediate the reinforcing enhancing properties of nicotine. Here, we used behavioral economic procedures to generate demand curves for consumption of the synthetic, short-acting, μ-opioid receptor agonist remifentanil (RMF) in adulthood following prior adolescent nicotine exposure (ANE) and again following reintroduction of acute nicotine administration (ANA). We found that ANE was sufficient to augment multiple indices of the motivational value of RMF in adulthood and these effects were further exacerbated by ANA given during RMF self-administration sessions. Additionally, we demonstrate that systemic antagonism of ORX1Rs with SB-334867 is more efficacious in limiting motivation for RMF in nicotine-exposed rats relative to controls and this differential efficacy was even greater in ANA conditions relative to former ANE. These findings support that nicotine-induced facilitation of orexin signaling may mechanistically contribute to augmented opioid consumption offering critical insight for treatment options for a population that is particularly vulnerable to developing opioid use disorder.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.