Abstract：
:Tobacco smoke exposure has been shown to inhibit brain and platelet MAO B in animals and in humans. Though the mechanism(s) responsible for MAO B inhibition are not known, studies in rodents have shown that nicotine administration does not inhibit brain MAO B. In this study we investigated whether brain MAO B is also unaffected by nicotine in the living primate. Brain MAO B was measured with positron emission tomography (PET) and deuterium substituted [11C]L-deprenyl ([11C]L-deprenyl-D2) in three baboons at baseline and 5 minutes after the injection of (-)-nicotine (0.3 mg administered intravenously). A three-compartment model was used to calculate the plasma to brain transfer constant K1 which is related to blood flow, and lambda k3, which is a function of the concentration of catalytically active MAO B molecules. Nicotine administration did not produce significant changes in either of these parameters. This study in living baboons confirms previous studies in rodents and solidifies the notion that other mechanisms for MAO B inhibition observed in smokers need to be considered.
journal_name
Life Scijournal_title
Life sciencesauthors
Fowler JS,Volkow ND,Logan J,Pappas N,King P,MacGregor R,Shea C,Garza V,Gatley SJdoi
10.1016/s0024-3205(98)00251-3subject
Has Abstractpub_date
1998-01-01 00:00:00pages
PL19-23issue
2eissn
0024-3205issn
1879-0631pii
S0024-3205(98)00251-3journal_volume
63pub_type
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