In humans, nicotine is self administered by inhalation of tobacco smoke as
opposed to animal models, where nicotine is administered via systemic injec
tion. The aim of the present study was to clarify whether tobacco smoke inh
alation would affect dopaminergic projections differently from the reported
activation after the systemic administration of nicotine. For this purpose
, tobacco smoke from cigarettes containing 1.0 or 0.1 mg nicotine was deliv
ered by inhalation to rats, while recording from antidromically identified
nigrostriatal and mesolimbic dopamine neurons. Smoke inhalation from 1.0 mg
nicotine cigarettes caused a peculiar abrupt increase: of discharge activi
ty of mesolimbic dopamine neurons while nigrostriatal cells were less respo
nsive. This activation was promptly antagonized by mecamylamine (2.0 mg/kg,
i.v.). In contrast, smoke delivered from 0.1 mg nicotine cigarettes was in
effective. These findings suggest that the boosting activation of mesolimbi
c dopamine neurons by inhaled nicotine might be relevant for the rewarding
properties Of tobacco smoking and also for the effectiveness of new treatme
nts to stop smoking. NeuroReport 11:3637-3639 (C) 2000 Lippincott Williams
& Wilkins.