Occupancy of brain nicotinic acetylcholine receptors by nicotine doses equivalent to those obtained when smoking a cigarette

Functional brain imaging of tobacco use and dependence

“…In a 2-FA PET study (Valette et al, 2003), IV nicotine (0.6 mg), inhalation of tobacco smoke from one cigarette (0.9 mg nicotine), and IV nornicotine were all found to reduce the volume of distribution of the tracer by roughly 30-60% in the thalamus and putamen at 80 min, and this reduction of 2-FA binding was relatively long-lived (up to 6 h). Similarly, a 50% reduction in nAChR availability was found with IV nicotine administration to baboons using an epibatidine analog and PET scanning (Ding et al, 2000). Taken together, these studies demonstrate that radiotracers for nAChRs can be administered safely to measure nAChR densities, and that nicotine and smoking substantially decrease α 4 β 2 nAChR availability.…”

Long‐lasting occupancy of central nicotinic acetylcholine receptors after smoking: a PET study in monkeys

“…The anaesthetic agent, isoflurane, used in Ding's (2000) and in the present studies, increased the affinity of α4β2 nAChRs (Raines and Zachariah 2000) by desensitizing them, and therefore could modify the kinetics of nicotine either administered i.v. or during smoking.…”

Temporal Change in Human Nicotinic Acetylcholine Receptor After Smoking Cessation: 5IA SPECT Study

“…Thus, we would expect some level of nicotine or metabolites in the brain that would compete with 123 I-5IA and impair imaging of the upregulation of nAChRs. Also, we believe that some level of nicotine in the brain resulted in a high level of occupancy of the receptors, which reduced specific tracer uptake (27). Because of competitive binding between the radioligand and nicotine in the brain, imaging of upregulation of nAChRs in vivo requires sufficient time for nicotine clearance (.4-h smoking cessation).…”