Effects of the nicotinic agonist varenicline, nicotinic antagonist r-bPiDI, and DAT inhibitor (R)-modafinil on co-use of ethanol and nicotine in ... View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2018-05

AUTHORS

Sarah E. Maggio, Meredith A. Saunders, Thomas A. Baxter, Kimberly Nixon, Mark A. Prendergast, Guangrong Zheng, Peter Crooks, Linda P. Dwoskin, Rachel D. Slack, Amy H. Newman, Richard L. Bell, Michael T. Bardo

ABSTRACT

RATIONALE: Co-users of alcohol and nicotine are the largest group of polysubstance users worldwide. Commonalities in mechanisms of action for ethanol (EtOH) and nicotine proposes the possibility of developing a single pharmacotherapeutic to treat co-use. OBJECTIVES: Toward developing a preclinical model of co-use, female alcohol-preferring (P) rats were trained for voluntary EtOH drinking and i.v. nicotine self-administration in three phases: (1) EtOH alone (0 vs. 15%, two-bottle choice), (2) nicotine alone (0.03 mg/kg/infusion, active vs. inactive lever), and (3) concurrent access to both EtOH and nicotine. Using this model, we examined the effects of (1) varenicline, a nicotinic acetylcholine receptor (nAChR) partial agonist with high affinity for the α4β2* subtype; (2) r-bPiDI, a subtype-selective antagonist at α6β2* nAChRs; and (3) (R)-modafinil, an atypical inhibitor of the dopamine transporter (DAT). RESULTS: In phases 1 and 2, pharmacologically relevant intake of EtOH and nicotine was achieved. In the concurrent access phase (phase 3), EtOH consumption decreased while nicotine intake increased relative to phases 1 and 2. For drug pretreatments, in the EtOH access phase (phase 1), (R)-modafinil (100 mg/kg) decreased EtOH consumption, with no effect on water consumption. In the concurrent access phase, varenicline (3 mg/kg), r-bPiDI (20 mg/kg), and (R)-modafinil (100 mg/kg) decreased nicotine self-administration but did not alter EtOH consumption, water consumption, or inactive lever pressing. CONCLUSIONS: These results indicate that therapeutics which may be useful for smoking cessation via selective inhibition of α4β2* or α6β2* nAChRs, or DAT inhibition, may not be sufficient to treat EtOH and nicotine co-use. More... »

PAGES

1439-1453

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1007/s00213-018-4853-4

    DOI

    http://dx.doi.org/10.1007/s00213-018-4853-4

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1101093810

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/29455292


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    HOW TO GET THIS DATA PROGRAMMATICALLY:

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    curl -H 'Accept: application/rdf+xml' 'https://scigraph.springernature.com/pub.10.1007/s00213-018-4853-4'


     

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