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Mapping Human Brain Monoamine Oxidase A and B with $^{11}$C-Labeled Suicide Inactivators and PET

J. S. Fowler, R. R. MacGregor, A. P. Wolf, C. D. Arnett, S. L. Dewey, D. Schlyer, D. Christman, J. Logan, M. Smith, H. Sachs, S. M. Aquilonius, P. Bjurling, C. Halldin, P. Hartvig, K. L. Leenders, H. Lundqvist, L. Oreland, C.-G. Stålnacke and B. Långström
Science
New Series, Vol. 235, No. 4787 (Jan. 23, 1987), pp. 481-485
Stable URL: http://www.jstor.org/stable/1698351
Page Count: 5
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Mapping Human Brain Monoamine Oxidase A and B with $^{11}$C-Labeled Suicide Inactivators and PET
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Abstract

The regional distributions of monoamine oxidase (MAO) types A and B have been identified in human brain in vivo with intravenously injected $^{11}$C-labeled suicide enzyme inactivators, clorgyline and L-deprenyl, and positron emission tomography. The rapid brain uptake and retention of radioactivity for both $^{11}$C tracers indicated irreversible trapping. The anatomical distribution of $^{11}$C the distribution of MAO A and MAO B in human brain in autopsy material. The corpus striatum, thalamus, and brainstem contained high MAO activity. The magnitudes of uptake of both [$^{11}$C]clorgyline and L-[$^{11}$C]deprenyl were markedly reduced in one subject treated with the antidepressant MAO inhibitor phenelzine. A comparison of the brain uptake and retention of the $^{11}$C-labeled inactive (D-) and active (L-) enantiomers of deprenyl showed rapid clearance of the inactive enantiomer and retention of the active enantiomer within MAO B-rich brain structures, in agreement with the known stereoselectivity of MAO B for L-deprenyl. Prior treatment with unlabeled L-deprenyl prevented retention of L-[$^{11}$C]deprenyl. Thus, suicide enzyme inactivators labeled with positron emitters can be used to quantitate the distribution and kinetic characteristics of MAO in human brain structures.

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