Abstract
Alcohol and nicotine are frequently co‐abused drugs affecting millions of people in the US and other parts of world. Previous research suggests that high incidence rates of smoking are associated with increased alcohol consumption contributing a major risk factor for alcohol relapse. Accumulated evidence indicates that brain nicotinic receptors (nAChRs) are common points of action for nicotine‐alcohol (ethanol) interactions. Thus targeting nAChRs could be a potential strategy for the management of nicotine‐ethanol co‐dependence. The present study examined the effects of cytisine, a nAChR partial agonist, on chronic nicotine‐induced ethanol intake in C57BL/6J mice. After establishment of ethanol (10%, v/v) preference using two‐bottle choice continuous drinking procedure, mice received subcutaneous injections of saline, nicotine (0.4 mg/kg) or cytisine (0.5, 1.5 or 3 mg/kg) given before nicotine treatment for 10 days. Chronic nicotine treatment significantly increased ethanol intake (g/kg) post 1 h (166%; p < 0.05) and 2 h (152%; p < 0.05) compared to saline. Pretreatment with cytisine (0.5 or 1.5 mg/kg) significantly reduced nicotine‐induced ethanol intake post 1 h (32% or 43% respectively; p < 0.005) and 2 h (50% or 53% respectively; p < 0.005). These results further suggest that brain nAChRs localized in mid‐brain dopamine system are ideal therapeutic targets in regulating ethanol and nicotine consumption. Thus, development of cytisine or new analogs would be a potential pharmacological strategy for the treatment of nicotine‐alcohol co‐dependence. (Supported in part by SDSU Research grant).
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call