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Evaluation of (-)-[18 F]Flubatine-specific binding: Implications for reference region approaches
Shivani Bhatt1,2, Ansel T Hillmer2,3,4, Nabeel Nabulsi2
1Interdepartmental Neuroscience Program, Yale University School of Medicine, New Haven, Connecticut.
Synapse (New York, N.Y.)
|November 7, 2017
Summary
Smoking tobacco cigarettes displaces (-)-[18 F]Flubatine binding to α4 β2 *-nicotinic acetylcholine receptors (α4 β2 *-nAChRs) in the brain. This finding impacts how researchers quantify receptor changes using this PET tracer.
Area of Science:
- Neuroscience
- Radiochemistry
- Pharmacology
Background:
- α4 β2 *-nicotinic acetylcholine receptors (α4 β2 *-nAChRs) are key targets for nicotine.
- Understanding nicotine's effects on these receptors is crucial for addiction research.
Purpose of the Study:
- To characterize changes in (-)-[18 F]Flubatine binding to α4 β2 *-nAChRs during a smoking challenge.
- To assess the impact of smoking on tracer binding in various brain regions.
Main Methods:
- Positron emission tomography (PET) imaging with (-)-[18 F]Flubatine infusion in three smokers.
- Tobacco cigarette smoking initiated during the PET scan.
- Equilibrium analysis to quantify changes in distribution volume (VT) before and after smoking.
Main Results:
- Smoking significantly reduced (-)-[18 F]Flubatine binding (VT) in multiple brain regions, including corpus callosum (21%), frontal cortex (17%), cerebellum (36%), and putamen (22%).
- Displaceable binding was observed throughout the brain, particularly in the corpus callosum.
Conclusions:
- Tobacco smoking displaces (-)-[18 F]Flubatine binding to α4 β2 *-nAChRs.
- Reference region-based quantification using the corpus callosum requires careful validation of displaceable binding and nondisplaceable kinetics.
