Differential trace amine alterations in individuals receiving acetylenic inhibitors of MAO-A (clorgyline) or MAO-B (selegiline and pargyline)

  • D. L. Murphy
  • F. Karoum
  • D. Pickar
  • R. M. Cohen
  • S. Lipper
  • A. M. Mellow
  • P. N. Tariot
  • T. Sunderland
Part of the Journal of Neural Transmission. Supplement book series (NEURAL SUPPL, volume 52)


Marked, dose-dependent elevations in the urinary excretion of phenylethylamine, para-tyramine, and meta-tyramine were observed in depressed patients treated for three or more weeks with 10, 30, or 60 mg/ day of the partially-selective inhibitor of MAO-B, selegiline (1-deprenyl). In comparative studies with other, structurally similar acetylenic inhibitors of MAO, pargyline, an MAO-B > MAO-A inhibitor used in doses of 90mg/day for three or more weeks, produced elevations in these trace amines which were similar to those found with the highest dose of selegiline studied. Clorgyline, a selective inhibitor of MAO-A used in doses of 30mg/ day for three or more weeks (a dose/time regimen previously reported to reduce urinary, plasma, and cerebrospinal fluid 3-methoxy-4hydroxyphenylethyleneglycol (MHPG) > 80%, indicating a marked inhibitory effect on MAO-A in humans in vivo) produced negligible changes in trace amine excretion. In comparison to recent studies of individuals lacking the genes for MAO-A, MAO-B, or both MAO-A and MAO-B, the lack of change in trace amine excretion in individuals with a mutation affecting only MAO-A is in agreement with the observed lack of effect of clorgyline in the present study. Selegiline produced larger changes in trace amines — at least at the higher doses studied — than found in individuals lacking the gene for MAO-B, in agreement with other data suggesting a lesser selectivity for MAO-B inhibition when selegiline was given in doses higher than 10mg/day. Overall, trace amine elevations in individuals receiving the highest dose of deprenyl or receiving pargyline were approximately three to five-fold lower than the elevations observed in individuals lacking the genes for both MAOA and MAO-B, suggesting that these drug doses yield incomplete inhibition of MAO-A and MAO-B.


Monoamine Oxidase Trace Amine Deficient Subject Norrie Disease Inhibitor Clorgyline 
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Copyright information

© Springer-Verlag Wien 1998

Authors and Affiliations

  • D. L. Murphy
    • 1
    • 8
  • F. Karoum
    • 2
  • D. Pickar
    • 3
  • R. M. Cohen
    • 4
  • S. Lipper
    • 5
  • A. M. Mellow
    • 6
  • P. N. Tariot
    • 7
  • T. Sunderland
    • 1
  1. 1.Laboratory of Clinical ScienceNational Institute of Mental HealthBethesdaUSA
  2. 2.Neuroscience Center, St. Elizabeth’s HospitalNational Institute of Mental HealthUSA
  3. 3.Experimental Therapeutics BranchNational Institute of Mental HealthBethesdaUSA
  4. 4.Laboratory of Cerebral MetabolismNational Institute of Mental HealthBethesdaUSA
  5. 5.Department of PsychiatryDuke University School of MedicineDurhamUSA
  6. 6.Department of PsychiatryUniversity of Michigan School of MedicineAnn ArborUSA
  7. 7.Department of PsychiatryUniversity of Rochester Medical CenterRochesterUSA
  8. 8.Laboratory of Clinical ScienceNIMH, NIH Clinical Center, 10-3D41BethesdaUSA

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