An acute dose of nicotine does not inhibit MAO B in baboon brain in vivo

Joanna S. Fowler, Nora D. Volkow, Jean Logan, Naomi Pappas, Payton King, Robert MacGregor, Colleen Shea, Victor Garza, S. John Gatley

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43 Scopus citations


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 λk3, 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.

Original languageEnglish
Pages (from-to)PL19-PL23
JournalLife Sciences
Issue number2
StatePublished - 5 Jun 1998
Externally publishedYes


  • MAO B
  • Nicotine
  • Positron emission tomography
  • Tobacco smoke


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