Resumo

Introduction: There is a lack of experimental studies that investigate the effects of tobacco smoke exposure during adolescence. Nicotine is considered as the most important psychoactive substance present in tobacco and the one responsible for tobacco addiction. Nicotine indirectly affects a wide variety of neurotransmitter systems; however, as an acetylcholine analog, the ionotropic nicotinic acetylcholine receptors (nAChRs) are the primary cellular mediators of its effects. Here, we investigated the effects of tobacco smoke generated from cigarettes containing either high or low levels of nicotine on the cholinergic system. Methods: From postnatal day (PN) 30 to 45, 18 C57BL/6 (inbred) and 16 Swiss (outbred) mice of both sexes were exposed to tobacco smoke (whole body exposure for 8 hr/day and 7 days/week) generated from one of two reference research cigarettes: type 3R4F (HighNIC group—nicotine = 0.73 mg/cigarette) or type 4A1 (LowNIC group—nicotine = 0.14 mg/cigarette). Control mice (CT) were exposed to air. On PN 45, cotinine (nicotine metabolite) serum levels and [3H]choline uptake in the cerebral cortex and hippocampus were assessed. Results: Cotinine serum levels were eight times higher in HighNIC mice (C57BL/6:142.0 ± 16.7 ng/ml and Swiss: 197.6 ± 11.1 ng/ml) when compared with LowNIC ones (C57BL/6:17.4 ± 7.4 ng/ml and Swiss: 24.6 ± 2.2 ng/ml). Only HighNIC mice presented a significant increase in [3H]choline uptake in the hippocampus (C57BL/6: HighNIC > CT and HighNIC > LowNIC, p < .001 and Swiss: HighNIC > CT and HighNIC > LowNIC, p < .001), whereas in the cerebral cortex, both HighNIC and LowNIC mice presented increased [3H]choline uptake (C57BL/6: HighNIC > CT and LowNIC > CT, p < .05 and Swiss: HighNIC > CT and LowNIC > CT, p < .001). Conclusion: The present findings suggest that even low nicotine levels, when combined to other components of cigarette smoke, interfere with the cholinergic function. These facts claim attention to the possibility that attributing the effects of tobacco smoke exclusively to nicotine might constitute an oversimplified view and that future experimental studies on tobacco components, combined or not to nicotine, are warranted. Our results indicate that tobacco smoke exposure during adolescence increases [3H]choline uptake. However, the effects are dependent on the type of cigarette and on the brain region.