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Dynamic, adaptive changes in MAO-A binding after alterations in substrate availability: An in vivo [(11)C]-harmine positron emission tomography study

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Sacher,  Julia
Vivian M. Rakoff PET Centre, Centre for Addiction and Mental Health, University of Toronto, ON, Canada;
Mood and Anxiety Disorders Division, Centre for Addiction and Mental Health, University of Toronto, ON, Canada;
Clinic for Cognitive Neurology, University of Leipzig, Germany;
Department Neurology, MPI for Human Cognitive and Brain Sciences, Max Planck Society;

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Citation

Sacher, J., Rabiner, E. A., Clark, M., Rusjan, P., Soliman, A., Boskovic, R., et al. (2012). Dynamic, adaptive changes in MAO-A binding after alterations in substrate availability: An in vivo [(11)C]-harmine positron emission tomography study. Journal of Cerebral Blood Flow and Metabolism, 32(3), 443-446. doi:10.1038/jcbfm.2011.184.


Cite as: http://hdl.handle.net/11858/00-001M-0000-000F-43B8-0
Abstract
Monoamine oxidase A (MAO-A) is an important target in the pathophysiology and therapeutics of major depressive disorder, aggression, and neurodegenerative conditions. We measured the effect of changes in MAO-A substrate on MAO-A binding in regions implicated in affective and neurodegenerative disease with [11C]-harmine positron emission tomography in healthy volunteers. Monoamine oxidase A VT, an index of MAO-A density, was decreased (mean: 14%±9%) following tryptophan depletion in prefrontal cortex (P<0.031), and elevated (mean: 17%±11%) in striatum following carbidopa–levodopa administration (P<0.007). These findings suggest an adaptive role for MAO-A in maintaining monoamine neurotransmitter homeostasis by rapidly compensating fluctuating monoamine levels.